Appendix 2-5: Rejected ecotox bibliography for Chlorpyrifos



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This attraction response was not altered by a previous 4-d exposure to lower concentrations of the mixtures, suggesting fish will not learn from previous exposures. However, previous exposures did alter an attraction response to an amino acid prevalent in food (L-alanine). The present study demonstrates that fish living within urban waterways may elect to place themselves in herbicide-contaminated environments and that these exposures may alter their behavioral responses to cues necessary for survival. Environ. Toxicol. Chem. 2011;30:2046-2054. (C) 2011 SETAC
Keywords: Zebrafish, Herbicide avoidance, Behavioral attraction, 2,4-D, Glyphosate
ISI Document Delivery No.: 813AH

1379. Tighe, A.; Ray-Sinha, A.; Staples, O. D., and Taylor, S. S. Gsk-3 Inhibitors Induce Chromosome Instability.


Rec #: 51409
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: EMBO J. 2003 Jun 2;22(11):2752-63 (medline /12773390)
COMMENTS: Cites: J Biol Chem. 2003 Nov 14;278(46):45937-45 (medline /12928438)
COMMENTS: Cites: Science. 2003 Sep 12;301(5639):1547-50 (medline /12970569)
COMMENTS: Cites: J Biol Chem. 2003 Dec 19;278(51):51786-95 (medline /14523000)
COMMENTS: Cites: Mol Cell. 2003 Aug;12(2):381-92 (medline /14536078)
COMMENTS: Cites: Curr Opin Cell Biol. 2003 Dec;15(6):672-83 (medline /14644191)
COMMENTS: Cites: J Cell Biol. 2003 Dec 8;163(5):949-61 (medline /14662741)
COMMENTS: Cites: Bioorg Med Chem Lett. 2004 Jan 19;14(2):413-6 (medline /14698171)
COMMENTS: Cites: J Cell Biol. 2000 May 15;149(4):761-6 (medline /10811817)
COMMENTS: Cites: Nature. 2000 Jul 6;406(6791):86-90 (medline /10894547)
COMMENTS: Cites: Chem Biol. 2000 Oct;7(10):793-803 (medline /11033082)
COMMENTS: Cites: Mol Med Today. 2000 Dec;6(12):462-9 (medline /11099951)
COMMENTS: Cites: Curr Biol. 2001 Jan 9;11(1):44-9 (medline /11166179)
COMMENTS: Cites: Nat Cell Biol. 2001 Apr;3(4):429-32 (medline /11283619)
COMMENTS: Cites: Nat Cell Biol. 2001 Apr;3(4):433-8 (medline /11283620)
COMMENTS: Cites: Diabetes. 2001 May;50(5):937-46 (medline /11334436)
COMMENTS: Cites: EMBO Rep. 2001 Jul;2(7):609-14 (medline /11454737)
COMMENTS: Cites: Nat Rev Mol Cell Biol. 2001 Oct;2(10):769-76 (medline /11584304)
COMMENTS: Cites: J Cell Sci. 2001 Dec;114(Pt 24):4385-95 (medline /11792804)
COMMENTS: Cites: J Med Chem. 2002 Mar 14;45(6):1292-9 (medline /11881998)
COMMENTS: Cites: Nat Rev Mol Cell Biol. 2002 May;3(5):328-38 (medline /11988767)
COMMENTS: Cites: Bioorg Med Chem Lett. 2002 Jun 3;12(11):1525-8 (medline /12031334)
COMMENTS: Cites: Genes Dev. 2004 Jan 1;18(1):48-61 (medline /14724178)
COMMENTS: Cites: J Cell Biol. 2004 Jan 19;164(2):243-53 (medline /14734535)
COMMENTS: Cites: J Cell Sci. 1992 Nov;103 ( Pt 3):665-75 (medline /1478963)
COMMENTS: Cites: J Cell Sci. 2004 Mar 1;117(Pt 7):1117-28 (medline /14970257)
COMMENTS: Cites: J Cell Sci. 2004 Mar 15;117(Pt 8):1577-89 (medline /15020684)
COMMENTS: Cites: Mol Biol Cell. 2004 Jun;15(6):2978-91 (medline /15075372)
COMMENTS: Cites: Trends Biochem Sci. 2004 Feb;29(2):95-102 (medline /15102436)
COMMENTS: Cites: EMBO J. 2004 Jun 2;23(11):2235-45 (medline /15152189)
COMMENTS: Cites: Chromosoma. 2004 Jun;112(8):389-97 (medline /15156327)
COMMENTS: Cites: Bioorg Med Chem. 2004 Jun 15;12(12):3167-85 (medline /15158785)
COMMENTS: Cites: Nat Rev Drug Discov. 2004 Jun;3(6):479-87 (medline /15173837)
COMMENTS: Cites: Chromosome Res. 2004;12(6):599-616 (medline /15289666)
COMMENTS: Cites: Annu Rev Cell Dev Biol. 2004;20:337-66 (medline /15473844)
COMMENTS: Cites: J Cell Sci. 2004 Nov 1;117(Pt 23):5461-77 (medline /15509863)
COMMENTS: Cites: J Cell Sci. 2004 Dec 15;117(Pt 26):6339-53 (medline /15561772)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2005 Mar 22;102(12):4365-70 (medline /15767571)
COMMENTS: Cites: Science. 2005 Mar 25;307(5717):1904-9 (medline /15790842)
COMMENTS: Cites: Mol Biol Cell. 2005 Oct;16(10):4609-22 (medline /16030254)
COMMENTS: Cites: J Cell Sci. 2005 Aug 15;118(Pt 16):3639-52 (medline /16046481)
COMMENTS: Cites: Trends Cell Biol. 2005 Sep;15(9):486-93 (medline /16084093)
COMMENTS: Cites: Gene. 2005 Nov 21;361:1-12 (medline /16185824)
COMMENTS: Cites: Nat Rev Cancer. 2005 Oct;5(10):773-85 (medline /16195750)
COMMENTS: Cites: Trends Cell Biol. 2005 Nov;15(11):589-98 (medline /16214339)
COMMENTS: Cites: J Cell Sci. 2005 Oct 15;118(Pt 20):4889-900 (medline /16219694)
COMMENTS: Cites: J Cell Biol. 2005 Oct 24;171(2):197-200 (medline /16247021)
COMMENTS: Cites: Nature. 2006 Apr 13;440(7086):954-8 (medline /16612388)
COMMENTS: Cites: EMBO J. 2006 Jun 21;25(12):2814-27 (medline /16763565)
COMMENTS: Cites: J Cell Sci. 2006 Sep 1;119(Pt 17):3664-75 (medline /16912073)
COMMENTS: Cites: Science. 2006 Oct 13;314(5797):268-74 (medline /16959974)
COMMENTS: Cites: J Cell Biol. 2007 Jan 15;176(2):183-95 (medline /17227893)
COMMENTS: Cites: Eur J Biochem. 1983 Jan 17;130(1):227-34 (medline /6402364)
COMMENTS: Cites: Cancer Res. 1995 Jul 15;55(14):2972-7 (medline /7606712)
COMMENTS: Cites: J Cell Biol. 1995 Aug;130(4):941-8 (medline /7642709)
COMMENTS: Cites: J Cell Biol. 1995 Jun;129(5):1195-204 (medline /7775567)
COMMENTS: Cites: Nature. 1995 Feb 16;373(6515):630-2 (medline /7854422)
COMMENTS: Cites: J Cell Biol. 1994 Dec;127(5):1301-10 (medline /7962091)
COMMENTS: Cites: Mol Cell Biol. 1994 Jan;14(1):831-9 (medline /8264650)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1996 Aug 6;93(16):8455-9 (medline /8710892)
COMMENTS: Cites: Curr Biol. 1996 Dec 1;6(12):1664-8 (medline /8994831)
COMMENTS: Cites: Science. 1997 Jan 31;275(5300):632-7 (medline /9005842)
COMMENTS: Cites: Cell. 1997 May 30;89(5):727-35 (medline /9182760)
COMMENTS: Cites: J Cell Sci. 1998 Mar;111 ( Pt 5):557-72 (medline /9454730)
COMMENTS: Cites: Diabetes. 2002 Oct;51(10):2903-10 (medline /12351425)
COMMENTS: Cites: Nat Rev Mol Cell Biol. 2002 Oct;3(10):731-41 (medline /12360190)
COMMENTS: Cites: Curr Biol. 2002 Dec 10;12(23):2055-9 (medline /12477396)
COMMENTS: Cites: J Cell Sci. 2003 Feb 15;116(Pt 4):637-46 (medline /12538764)
COMMENTS: Cites: Cell. 2003 Feb 21;112(4):407-21 (medline /12600307)
COMMENTS: Cites: Diabetes. 2003 Mar;52(3):588-95 (medline /12606497)
COMMENTS: Cites: J Cell Sci. 2003 Apr 1;116(Pt 7):1175-86 (medline /12615961)
COMMENTS: Cites: J Cell Biol. 2003 Apr 28;161(2):267-80 (medline /12719470)
ABSTRACT: BACKGROUND: Several mechanisms operate during mitosis to ensure accurate chromosome segregation. However, during tumour evolution these mechanisms go awry resulting in chromosome instability. While several lines of evidence suggest that mutations in adenomatous polyposis coli (APC) may promote chromosome instability, at least in colon cancer, the underlying mechanisms remain unclear. Here, we turn our attention to GSK-3 - a protein kinase, which in concert with APC, targets beta-catenin for proteolysis - and ask whether GSK-3 is required for accurate chromosome segregation.
ABSTRACT: RESULTS: To probe the role of GSK-3 in mitosis, we inhibited GSK-3 kinase activity in cells using a panel of small molecule inhibitors, including SB-415286, AR-A014418, 1-Azakenpaullone and CHIR99021. Analysis of synchronised HeLa cells shows that GSK-3 inhibitors do not prevent G1/S progression or cell division. They do, however, significantly delay mitotic exit, largely because inhibitor-treated cells have difficulty aligning all their chromosomes. Although bipolar spindles form and the majority of chromosomes biorient, one or more chromosomes often remain mono-oriented near the spindle poles. Despite a prolonged mitotic delay, anaphase frequently initiates without the last chromosome aligning, resulting in chromosome non-disjunction. To rule out the possibility of "off-target" effects, we also used RNA interference to selectively repress GSK-3beta. Cells deficient for GSK-3beta exhibit a similar chromosome alignment defect, with chromosomes clustered near the spindle poles. GSK-3beta repression also results in cells accumulating micronuclei, a hallmark of chromosome missegregation.
ABSTRACT: CONCLUSION: Thus, not only do our observations indicate a role for GSK-3 in accurate chromosome segregation, but they also raise the possibility that, if used as therapeutic agents, GSK-3 inhibitors may induce unwanted side effects by inducing chromosome instability.
MESH HEADINGS: Cell Line, Tumor
MESH HEADINGS: *Chromosomal Instability
MESH HEADINGS: *Chromosome Segregation
MESH HEADINGS: Glycogen Synthase Kinase 3/*antagonists &
MESH HEADINGS: inhibitors/*metabolism
MESH HEADINGS: HeLa Cells
MESH HEADINGS: Humans
MESH HEADINGS: Mitosis/drug effects
MESH HEADINGS: Mitotic Spindle Apparatus/drug effects
MESH HEADINGS: Protein Kinase Inhibitors/adverse effects/chemistry/metabolism/*pharmacology
MESH HEADINGS: RNA Interference
MESH HEADINGS: beta Catenin/metabolism eng

1380. Tirelli, V.; Catone, T.; Turco, L.; Di Consiglio, E.; Testai, E., and De Angelis, I. Effects of the pesticide clorpyrifos on an in vitro model of intestinal barrier. 2007; 21, (2): 308-313.


Rec #: 70609
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: Clorpyrifos (CPF), one of the most widely used organophosphorothionate pesticide can be detected as residues in food and drinking water; therefore the oral route is the major route of exposure for the general population, including children, following household use of this insecticide. Aim of this work was to investigate the possible acute cytotoxic effects of CPF on intestine and the integrity of the epithelial barrier, using Caco-2/TC7 cells as intestinal in vitro model. High level of CPF found inside the cells, corresponding to about 80% of the nominal concentration tested (30, 50 and 250 mu M), chosen as representative of the concentrations attainable in the intestinal lumen after actual levels of human oral exposure. In these conditions, no cytotoxicity in terms of cellular viability was observed. However, at the highest CPF nominal concentration (250 M) the impairment of barrier integrity was evidenced, due only to the parent compound, since no CPF metabolites could be detected in our experimental conditions. CPF itself was demonstrated to interfere with the tight junction on this in vitro model of epithelial intestinal cells, altering the barrier integrity and very likely the absorption of other co-administered chemicals. (c) 2006 Elsevier Ltd. All rights reserved.
Keywords: clorpyrifos, Caco-2/TC7 cells, intestinal barrier
ISI Document Delivery No.: 154HZ

1381. Tiryaki, Osman; Baysoyu, Dilan; Secer, Emine; Aydin, Guelizar, and Tiryaki, Osman. Testing the Stability of Pesticides During Sample Processing for the Chlorpyrifos and Malathion Residue Analysis in Cucumber, Including Matrix Effects. 2008 Jan; 80, (1): 38-43.


Rec #: 42319
Keywords: FOOD
Notes: Chemical of Concern: CPY
Abstract: Abstract: This article describes the procedure of the testing the stability of compounds during sample processing for the pesticide residue analysis in cucumber, including matrix matched assessment. To find out significant differences, one-tailed t test was applied to the data at 95% confidence level. Our results showed that the calculated value was bigger than the critical value (t sub(calc) > t sub(crit)), which means the pesticides were decomposed under our processing conditions.
Keywords: Chlorpyrifos
Keywords: T-cell receptor
Keywords: Data processing
Keywords: Pesticide residues
Keywords: Pesticides
Keywords: Toxicology Abstracts; Pollution Abstracts
Keywords: X 24330:Agrochemicals
Keywords: P 6000:TOXICOLOGY AND HEALTH
Keywords: Malathion
Keywords: Environmental Studies
Date revised - 2012-09-01
Language of summary - English
Pages - 38-43
ProQuest ID - 293872961
SubjectsTermNotLitGenreText - Chlorpyrifos; T-cell receptor; Data processing; Pesticide residues; Pesticides; Malathion
Last updated - 2012-11-08
Corporate institution author - Tiryaki, Osman; Baysoyu, Dilan; Secer, Emine; Aydin, Guelizar
DOI - OB-MD-0008051199; 8152639; 0007-4861 English

1382. Tiwari, M. K. and Guha, S. Role of Soil Organic Matter on the Sorption and Cosorption of Endosulfan and Chlorpyrifos on Agricultural Soils. 2012; 138, (4): 426-435.


Rec #: 70649
Keywords: FATE
Notes: Chemical of Concern: CPY
Abstract: Abstract: Sorption of endosulfan and chlorpyrifos was studied through batch experiments with three agricultural soils (organic carbon 0.8, 1.37, and 2%) and different initial concentrations of pesticides below the limits of their solubility. The effect of the presence of one pesticide on sorption of the other was also examined. The sorption of both pesticides followed the Lagergren kinetic model, and more than 95% of sorption was completed within 4-6 hours for endosulfan and 6-12 hours for chlorpyrifos. The equilibrium sorption of both pesticides was primarily on the soil organic matter, but the isotherms were nonlinear, especially at low-solute concentrations. The nonlinearity was the result of the sorption onto the hard carbon portion of soil organic carbon, which was also indicated by the simulations with a dual reactive domain model (DRDM). The sorption of either pesticide was suppressed in the presence of the other, and the isotherm nonlinearity decreased with increasing concentration of the cosolute. The effect of a cosolute was more prominent for the sorption of endosulfan compared with that of chlorpyrifos. The simulations with DRDM indicated a competitive sorption in the portion of organic carbon showing site-limited sorption. No competition was observed in the portion showing linear partition behavior. Among the two isomers of endosulfan, the beta isomer was preferentially partitioned over the alpha isomer. DOI: 10.1061/(ASCE)EE.1943-7870.0000490. (C) 2012 American Society of Civil Engineers.
Keywords: Endosulfan, Chlorpyrifos, Sorption, Pertition, Soil organic carbon,
ISI Document Delivery No.: 932AD

1383. Toccalino, Patricia L; Norman, Julia E; Scott, Jonathon C, and Toccalino, Patricia L. Chemical Mixtures in Untreated Water From Public-Supply Wells in the U.s. - Occurrence, Composition, and Potential Toxicity. 2012 Aug 1; 431, 262-270.


Rec #: 46589
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: Chemical mixtures are prevalent in groundwater used for public water supply, but little is known about their potential health effects. As part of a large-scale ambient groundwater study, we evaluated chemical mixtures across multiple chemical classes, and included more chemical contaminants than in previous studies of mixtures in public-supply wells. We (1) assessed the occurrence of chemical mixtures in untreated source-water samples from public-supply wells, (2) determined the composition of the most frequently occurring mixtures, and (3) characterized the potential toxicity of mixtures using a new screening approach. The U.S. Geological Survey collected one untreated water sample from each of 383 public wells distributed across 35 states, and analyzed the samples for as many as 91 chemical contaminants. Concentrations of mixture components were compared to individual human-health benchmarks; the potential toxicity of mixtures was characterized by addition of benchmark-normalized component concentrations. Most samples (84%) contained mixtures of two or more contaminants, each at concentrations greater than one-tenth of individual benchmarks. The chemical mixtures that most frequently occurred and had the greatest potential toxicity primarily were composed of trace elements (including arsenic, strontium, or uranium), radon, or nitrate. Herbicides, disinfection by-products, and solvents were the most common organic contaminants in mixtures. The sum of benchmark-normalized concentrations was greater than 1 for 58% of samples, suggesting that there could be potential for mixtures toxicity in more than half of the public-well samples. Our findings can be used to help set priorities for groundwater monitoring and suggest future research directions for drinking-water treatment studies and for toxicity assessments of chemical mixtures in water resources.
Keywords: Pollution monitoring
Keywords: P 2000:FRESHWATER POLLUTION
Keywords: geological surveys
Keywords: Toxicity
Keywords: Water supplies
Keywords: ENA 02:Toxicology & Environmental Safety
Keywords: Environmental Studies
Keywords: USA
Keywords: Environment Abstracts; Pollution Abstracts; Aqualine Abstracts; Water Resources Abstracts
Keywords: Water wells
Keywords: Chemical pollution
Keywords: Groundwater
Keywords: Benchmarks
Keywords: Drinking water
Date revised - 2012-11-01
Language of summary - English
Location - USA
Pages - 262-270
ProQuest ID - 1223021506
SubjectsTermNotLitGenreText - Pollution monitoring; geological surveys; Water wells; Chemical pollution; Toxicity; Drinking water; Benchmarks; Groundwater; Water supplies; USA
Last updated - 2012-12-06
Corporate institution author - Toccalino, Patricia L; Norman, Julia E; Scott, Jonathon C
DOI - OB-cfdc3f74-c5da-4aee-9091csamfg201; 16881475; 0048-9697 English

1384. Toma, L.; Menegon, M.; Romi, R.; De Matthaeis, E.; Montanari, M., and Severini, C. Status of insecticide resistance in Culex pipiens field populations from north-eastern areas of Italy before the withdrawal of OP compounds. 2011; 67, (1): 100-106.


Rec #: 70689
Keywords: SURVEY
Notes: Chemical of Concern: CPY
Abstract: Abstract: BACKGROUND: Heavy and constant use of organophosphorus (OP) larvicides selected Culex pipiens L. resistant populations through two main mechanisms of genetic resistance, the increased activity of detoxifying esterase and the production of alterate acetylcholinesterase-1 (AChE1) by G119S mutation. The aim of this study was the assessment of the distribution of Cx. pipiens populations resistant to temephos and chlorpyrifos in the north-eastern regions of Italy and the occurrence of the insensitive AChE in these populations. Data describe the situation in the last years before European legislation prohibited the use of OP larvicides in mosquito control, up until 2007. RESULTS: For the first time a high level of OP resistance in the samples from Ravenna (182-fold, 80% A4/B4 or A5/B5 esterases and 38.3% Ester(5)), Emilia Romagna region, was detected; therefore, new data from the Veneto and Friuli Venezia Giulia regions were obtained and reinforced existing knowledge about resistance previously studied along the Adriatic coast. Nearby, in the Villa Verucchio locality, the highest (87.5%) AChE1R was found. CONCLUSION: Cx. pipiens resistance esterases A5/B5 and A4/B4 spread southward along the Adriatic coastal plain while OPs were being used in mosquito control, as confirmed by the first molecular screening of the AChE1 gene in these populations. (C) 2010 Society of Chemical Industry
Keywords: insecticide resistance, Culex pipiens, esterases, acetylcholinesterase,
ISI Document Delivery No.: 701TV

1385. Tomkins, A. R.; Wilson, D. J., and Thomson, C. Thrip Control with Fluvalinate on Kiwifruit. SOIL; 1992; 45, 162-166.


Rec #: 1500
Keywords: MIXTURE
Call Number: NO MIXTURE (CPY,FYC,PSM,TAUF)
Notes: Chemical of Concern: CPY,FYC,PSM,TAUF

1386. Tope, A. M. and Rogers, P. F. Evaluation of protective effects of sulforaphane on DNA damage caused by exposure to low levels of pesticide mixture using comet assay. 2009; 44, (7): 657-662.


Rec #: 70709
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: The objective of the study was to evaluate the potential risk of DNA damage due to exposure to a mixture of the most widely used pesticides, namely endosulfan, chlorpyriphos and thiram at an environmentally relevant concentration (5 mu M each) and the DNA protective capacity of sulforaphane (SFN) (10-30 mu g/mL). DNA damage in human lymphocytes was ascertained with Single Cell Gel Electrophoresis (SCGE), also called Comet Assay. For positive control, H(2)O(2) at 100 mM was used. The pesticide mixture produced DNA damage at the concentration used in the lymphocytes. SFN was able to offer a statistically significant (P < 0.01), concentration-dependant protection to DNA damage between 10-20 mu g/mL in both the pre-incubation and co-incubation strategies. The results indicate that exposure to low levels of these pesticide mixtures can induce DNA damage, and the presence of SFN in diet may reduce the incidence of genetic damage, especially in farm workers. However, it is not clear whether SFN is involved in quenching of the free radicals generated by the pesticide mixture or it is involved in DNA repair mechanism.
Keywords: Pesticide mixture, DNA damage, human lymphocytes, sulforaphane, DNA
ISI Document Delivery No.: 535VY

1387. Toprak Karaman, Zerrin. Participation to the public life and becoming organized at local level in Romani settlements in Izmir. 2009 Apr; 26, (2): 308-321.


Rec #: 3870
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: There are more than 20 million Romani residents in many countries around the world. Due to social and economic reasons, many Romanies do not declare their ethnic origins; therefore, it is not possible to obtain any exact figures from official records. Romanies may have a preference of not defining themselves openly as ÇŁRomaniesÇĄ. However, it is thought that they are distinguished from non-Romanies with their unique behavior and speech. Actually, physical features cannot be used as a definite distinctive feature in identifying Romanies. As a matter of fact, the first Romanies who had entered Europe were identified by their dark skin color and black hair, whereas today, it is possible to see Romanies with light skin and hair color. Romanies and music are often considered together; they have trained numerous accomplished musicians.

zmir Metropolitan Municipality Area is covered as research area. -_zmir provincial population was 3,370,866 in 2000. The population of -_zmir Metropolitan Municipality Area (nine sub-provincial areas) was 2,232,265 in the 2000s. Gypsies/ Romani people/ Participation to the public life at local level/ Willingness of becoming organized/ Voting and the use of the right to be elected/ Cultural identities



1388. Torregrossa, M. M.; Corlett, P. R., and Taylor, J. R. Aberrant Learning and Memory in Addiction.
Rec #: 49899
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: Psychol Rev. 1982 Sep;89(5):529-72 (medline /7178332)
COMMENTS: Cites: J Pharmacol Exp Ther. 1996 Jan;276(1):306-15 (medline /8558448)
COMMENTS: Cites: Addiction. 1996 Jul;91(7):921-49; discussion 951-65 (medline /8688822)
COMMENTS: Cites: J Neurosci. 1997 Apr 15;17(8):2921-7 (medline /9092613)
COMMENTS: Cites: Behav Pharmacol. 1998 Jul;9(4):299-308 (medline /10065918)
COMMENTS: Cites: Curr Opin Neurobiol. 1999 Apr;9(2):195-202 (medline /10322181)
COMMENTS: Cites: Eur J Pharmacol. 1999 Jun 30;375(1-3):13-30 (medline /10443561)
COMMENTS: Cites: Addiction. 1999 Mar;94(3):327-40 (medline /10605857)
COMMENTS: Cites: Neuropsychopharmacology. 2001 Jan;24(1):66-74 (medline /11106877)
COMMENTS: Cites: Behav Neurosci. 2001 Apr;115(2):394-402 (medline /11345964)
COMMENTS: Cites: Biol Psychiatry. 2001 Jul 15;50(2):137-43 (medline /11526995)
COMMENTS: Cites: Addiction. 2002 Feb;97(2):155-67 (medline /11860387)
COMMENTS: Cites: Q J Exp Psychol B. 2002 Oct;55(4):331-48 (medline /12350285)
COMMENTS: Cites: Synapse. 2002 Dec 15;46(4):271-9 (medline /12373743)
COMMENTS: Cites: Neuropsychopharmacology. 2002 Dec;27(6):1006-15 (medline /12464457)
COMMENTS: Cites: Neuroscience. 2003;116(1):19-22 (medline /12535933)
COMMENTS: Cites: Behav Pharmacol. 2003 Mar;14(2):153-60 (medline /12658076)
COMMENTS: Cites: Neuropsychopharmacology. 2003 Jul;28(7):1264-71 (medline /12700688)
COMMENTS: Cites: Brain Res. 2003 Apr 25;970(1-2):214-20 (medline /12706263)
COMMENTS: Cites: J Neurosci. 2003 Apr 15;23(8):3531-7 (medline /12716962)
COMMENTS: Cites: Prog Neurobiol. 2003 Apr;69(6):375-90 (medline /12880632)
COMMENTS: Cites: Curr Opin Pharmacol. 2004 Feb;4(1):23-9 (medline /15018835)
COMMENTS: Cites: Behav Neurosci. 2004 Jun;118(3):505-13 (medline /15174928)
COMMENTS: Cites: J Mot Behav. 1981 Dec;13(4):262-73 (medline /15215073)
COMMENTS: Cites: Cereb Cortex. 2005 Mar;15(3):341-8 (medline /15269111)
COMMENTS: Cites: Arch Gen Psychiatry. 2004 Nov;61(11):1136-44 (medline /15520361)
COMMENTS: Cites: Curr Drug Targets CNS Neurol Disord. 2005 Oct;4(5):481-97 (medline /16266283)
COMMENTS: Cites: J Neurosci. 2006 Feb 1;26(5):1579-87 (medline /16452681)
COMMENTS: Cites: J Neurosci. 2006 Mar 15;26(11):3010-20 (medline /16540579)
COMMENTS: Cites: J Neurosci. 2006 Apr 5;26(14):3805-12 (medline /16597734)
COMMENTS: Cites: J Neurochem. 2006 Aug;98(3):905-15 (medline /16787418)
COMMENTS: Cites: Addiction. 2006 Aug;101(8):1153-66 (medline /16869845)
COMMENTS: Cites: Ann N Y Acad Sci. 2006 Jul;1071:521-4 (medline /16891611)
COMMENTS: Cites: Alcohol Clin Exp Res. 2006 Sep;30(9):1451-65 (medline /16930207)
COMMENTS: Cites: Eur J Neurosci. 2006 Nov;24(9):2643-53 (medline /17100852)
COMMENTS: Cites: CNS Spectr. 2007 Jan;12(1):51-6, 59-61 (medline /17192764)
COMMENTS: Cites: Behav Neurosci. 2007 Feb;121(1):212-7 (medline /17324065)
COMMENTS: Cites: Learn Mem. 2007 Mar;14(3):214-23 (medline /17353546)
COMMENTS: Cites: Eur J Neurosci. 2007 Apr;25(8):2260-8 (medline /17445224)
COMMENTS: Cites: Neuroreport. 2007 May 28;18(8):777-80 (medline /17471065)
COMMENTS: Cites: Biol Psychiatry. 2008 Feb 1;63(3):338-40 (medline /17719565)
COMMENTS: Cites: Behav Pharmacol. 2007 Sep;18(5-6):497-506 (medline /17762518)
COMMENTS: Cites: Behav Pharmacol. 2007 Nov;18(7):641-50 (medline /17912048)
COMMENTS: Cites: Behav Pharmacol. 2007 Nov;18(7):699-703 (medline /17912055)
COMMENTS: Cites: Exp Clin Psychopharmacol. 2007 Oct;15(5):461-71 (medline /17924780)
COMMENTS: Cites: Learn Mem. 2008 Feb;15(2):88-92 (medline /18235109)
COMMENTS: Cites: J Neurosci. 2008 Mar 19;28(12):3170-7 (medline /18354020)
COMMENTS: Cites: Behav Pharmacol. 2008 May;19(3):211-6 (medline /18469538)
COMMENTS: Cites: Science. 2008 Jun 6;320(5881):1352-5 (medline /18535246)
COMMENTS: Cites: Learn Mem. 2008 Sep;15(9):643-8 (medline /18772251)
COMMENTS: Cites: Alcohol Alcohol. 2008 Nov-Dec;43(6):626-9 (medline /18945754)
COMMENTS: Cites: Alcohol Clin Exp Res. 2009 Jan;33(1):139-49 (medline /18976347)
COMMENTS: Cites: Front Neurosci. 2008 Jul;2(1):86-99 (medline /18982111)
COMMENTS: Cites: Learn Mem. 2009 Jan;16(1):82-5 (medline /19144966)
COMMENTS: Cites: Behav Brain Res. 2009 May 16;199(2):345-9 (medline /19152811)
COMMENTS: Cites: Learn Mem. 2009 May;16(5):279-88 (medline /19380710)
COMMENTS: Cites: Pharmacol Biochem Behav. 2009 Sep;93(3):343-8 (medline /19490925)
COMMENTS: Cites: Neurobiol Learn Mem. 2009 Nov;92(4):544-51 (medline /19595781)
COMMENTS: Cites: Eur J Neurosci. 2009 Sep;30(5):889-900 (medline /19712099)
COMMENTS: Cites: Am J Drug Alcohol Abuse. 2009;35(6):434-8 (medline /20014913)
COMMENTS: Cites: Learn Mem. 2010 Apr;17(4):168-75 (medline /20332188)
COMMENTS: Cites: Eur J Pharmacol. 2006 Nov 21;550(1-3):95-106 (medline /17011546)
COMMENTS: Cites: Neurotoxicol Teratol. 2007 Jan-Feb;29(1):57-65 (medline /17184971)
COMMENTS: Cites: Eur Neuropsychopharmacol. 2007 Jul;17(8):532-40 (medline /17275266)
COMMENTS: Cites: Cereb Cortex. 2007 Dec;17(12):2820-7 (medline /17322558)
COMMENTS: Cites: Nat Rev Neurosci. 2007 Apr;8(4):262-75 (medline /17342174)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4147-52 (medline /17360491)
COMMENTS: Cites: Drug Alcohol Depend. 2007 Oct 8;90(2-3):193-202 (medline /17451890)
COMMENTS: Cites: Ann N Y Acad Sci. 2007 Dec;1121:610-38 (medline /17698993)
COMMENTS: Cites: Synapse. 2007 Dec;61(12):1002-5 (medline /17853433)
COMMENTS: Cites: Pharmacol Biochem Behav. 2008 Aug;90(2):261-72 (medline /17928041)
COMMENTS: Cites: Nat Neurosci. 2007 Nov;10(11):1398-400 (medline /17952068)
COMMENTS: Cites: J Neurosci. 2007 Nov 21;27(47):12967-76 (medline /18032670)
COMMENTS: Cites: Brain Res. 2008 Jan 16;1189:229-35 (medline /18067879)
COMMENTS: Cites: Eur J Pharmacol. 2008 Mar 17;582(1-3):78-87 (medline /18191832)
COMMENTS: Cites: PLoS One. 2008;3(1):e1506 (medline /18231593)
COMMENTS: Cites: Eur J Pharmacol. 2008 Apr 7;583(2-3):365-71 (medline /18275950)
COMMENTS: Cites: Nat Neurosci. 2008 Apr;11(4):514-20 (medline /18311134)
COMMENTS: Cites: Br J Pharmacol. 2008 May;154(2):327-42 (medline /18345022)
COMMENTS: Cites: Exp Clin Psychopharmacol. 2008 Apr;16(2):165-77 (medline /18489020)
COMMENTS: Cites: J Neurosci. 2008 May 21;28(21):5602-10 (medline /18495894)
COMMENTS: Cites: Philos Trans R Soc Lond B Biol Sci. 2008 Oct 12;363(1507):3233-43 (medline /18640922)
COMMENTS: Cites: Neuron. 2008 Jul 31;59(2):288-97 (medline /18667156)
COMMENTS: Cites: J Neurosci. 2008 Aug 13;28(33):8230-7 (medline /18701685)
COMMENTS: Cites: Neuropharmacology. 2009;56 Suppl 1:186-95 (medline /18708077)
COMMENTS: Cites: Nat Neurosci. 2008 Nov;11(11):1264-6 (medline /18849987)
COMMENTS: Cites: Neurosci Biobehav Rev. 2009 Mar;33(3):314-35 (medline /18955078)
COMMENTS: Cites: Pharmacol Biochem Behav. 2009 Mar;92(1):131-4 (medline /19032962)
COMMENTS: Cites: Learn Mem. 2008 Dec;15(12):857-65 (medline /19050157)
COMMENTS: Cites: J Neurosci. 2008 Dec 3;28(49):13248-57 (medline /19052216)
COMMENTS: Cites: Nat Neurosci. 2009 Feb;12(2):182-9 (medline /19136971)
COMMENTS: Cites: Biol Psychiatry. 2009 May 15;65(10):851-6 (medline /19181308)
COMMENTS: Cites: Nat Neurosci. 2009 Mar;12(3):256-8 (medline /19219038)
COMMENTS: Cites: Nat Rev Neurosci. 2009 Mar;10(3):224-34 (medline /19229241)
COMMENTS: Cites: J Neurosci. 2009 Mar 4;29(9):2876-84 (medline /19261883)
COMMENTS: Cites: Science. 2009 May 15;324(5929):951-5 (medline /19342552)
COMMENTS: Cites: Horm Behav. 2009 May;55(5):646-54 (medline /19446081)
COMMENTS: Cites: Eur J Neurosci. 2009 Jun;29(11):2225-32 (medline /19490086)
COMMENTS: Cites: J Neurosci. 2009 Jun 3;29(22):7191-8 (medline /19494141)
COMMENTS: Cites: Nature. 2009 Jul 9;460(7252):220-4 (medline /19536156)
COMMENTS: Cites: Trends Neurosci. 2009 Aug;32(8):413-20 (medline /19640595)
COMMENTS: Cites: Neuropsychopharmacology. 2010 Jan;35(2):357-67 (medline /19741593)
COMMENTS: Cites: Neuropsychopharmacology. 2010 Jan;35(1):48-69 (medline /19776734)
COMMENTS: Cites: Neuropsychopharmacology. 2010 Jan;35(2):388-400 (medline /19794408)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2009 Sep 29;106(39):16859-64 (medline /19805386)
COMMENTS: Cites: Nature. 2010 Jan 7;463(7277):49-53 (medline /20010606)
COMMENTS: Cites: J Behav Ther Exp Psychiatry. 2010 Jun;41(2):172-7 (medline /20060515)
COMMENTS: Cites: J Neurosci. 2010 Mar 24;30(12):4401-7 (medline /20335476)
COMMENTS: Cites: Ann N Y Acad Sci. 2010 Mar;1191:27-41 (medline /20392274)
COMMENTS: Cites: Behav Brain Funct. 2010;6:24 (medline /20416052)
COMMENTS: Cites: Behav Brain Res. 2010 Dec 1;213(2):201-7 (medline /20457186)
COMMENTS: Cites: J Neurosci. 2010 Jun 2;30(22):7749-53 (medline /20519550)
COMMENTS: Cites: Science. 2010 Jun 25;328(5986):1709-12 (medline /20576893)
COMMENTS: Cites: J Neurosci. 2010 Jul 7;30(27):9140-4 (medline /20610747)
COMMENTS: Cites: J Neurosci. 2010 Aug 4;30(31):10526-33 (medline /20685995)
COMMENTS: Cites: J Neurosci. 2010 Sep 1;30(35):11735-44 (medline /20810894)
COMMENTS: Cites: J Neurosci. 2010 Nov 17;30(46):15457-63 (medline /21084602)
COMMENTS: Cites: Nature. 2011 Jan 6;469(7328):53-7 (medline /21150898)
COMMENTS: Cites: Neuroscience. 2010 Sep 1;169(3):1127-35 (medline /20541592)
COMMENTS: Cites: J Exp Psychol Anim Behav Process. 1983 Jul;9(3):225-47 (medline /6153052)
COMMENTS: Cites: Psychopharmacology (Berl). 1984;84(3):405-12 (medline /6440188)
COMMENTS: Cites: J Exp Psychol Anim Behav Process. 1983 Jul;9(3):248-65 (medline /6886630)
COMMENTS: Cites: Psychol Rev. 1967 May;74(3):151-82 (medline /5342881)
COMMENTS: Cites: Psychol Rev. 1980 Nov;87(6):532-52 (medline /7443916)
COMMENTS: Cites: J Neurosci. 1994 Sep;14(9):5623-34 (medline /8083758)
COMMENTS: Cites: Brain Res Brain Res Rev. 1993 Sep-Dec;18(3):247-91 (medline /8401595)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1997 Sep 16;94(19):10397-402 (medline /9294222)
COMMENTS: Cites: J Neurosci. 1997 Nov 1;17(21):8443-50 (medline /9334416)
COMMENTS: Cites: J Neurosci. 1997 Nov 1;17(21):8491-7 (medline /9334421)
COMMENTS: Cites: Science. 1998 Dec 18;282(5397):2272-5 (medline /9856954)
COMMENTS: Cites: Eur J Neurosci. 1999 May;11(5):1598-604 (medline /10215912)
COMMENTS: Cites: Nature. 1999 Apr 15;398(6728):567-70 (medline /10217139)
COMMENTS: Cites: J Neurosci. 1999 May 15;19(10):4110-22 (medline /10234039)
COMMENTS: Cites: Ann N Y Acad Sci. 1999 Jun 29;877:412-38 (medline /10415662)
COMMENTS: Cites: Behav Brain Res. 2000 Jun 1;110(1-2):73-81 (medline /10802305)
COMMENTS: Cites: Annu Rev Neurosci. 2000;23:473-500 (medline /10845072)
COMMENTS: Cites: Am J Psychiatry. 2000 Nov;157(11):1789-98 (medline /11058476)
COMMENTS: Cites: Synapse. 2001 Mar 1;39(3):257-66 (medline /11169774)
COMMENTS: Cites: J Neurosci. 2001 Apr 1;21(7):2404-12 (medline /11264314)
COMMENTS: Cites: Nature. 2001 Mar 15;410(6826):376-80 (medline /11268215)
COMMENTS: Cites: J Neurochem. 2001 May;77(3):943-52 (medline /11331423)
COMMENTS: Cites: Nature. 2001 May 31;411(6837):583-7 (medline /11385572)
COMMENTS: Cites: J Neurosci. 2001 Oct 1;21(19):7831-40 (medline /11567074)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2001 Sep 25;98(20):11042-6 (medline /11572966)
COMMENTS: Cites: Brain Res Brain Res Rev. 2001 Oct;36(2-3):129-38 (medline /11690609)
COMMENTS: Cites: J Neurosci. 2001 Dec 1;21(23):9438-44 (medline /11717377)
COMMENTS: Cites: Nat Neurosci. 2002 Apr;5(4):348-55 (medline /11889468)
COMMENTS: Cites: Behav Neurosci. 2002 Feb;116(1):169-73 (medline /11895178)
COMMENTS: Cites: Neurosci Biobehav Rev. 2004 Oct;28(6):533-46 (medline /15527861)
COMMENTS: Cites: J Trauma Stress. 2004 Dec;17(6):485-96 (medline /15730067)
COMMENTS: Cites: Neuron. 2005 Sep 15;47(6):795-801 (medline /16157275)
COMMENTS: Cites: Biol Psychiatry. 2002 Nov 15;52(10):976-86 (medline /12437938)
COMMENTS: Cites: Synapse. 2003 Apr;48(1):10-7 (medline /12557267)
COMMENTS: Cites: J Neurosci. 2003 Feb 1;23(3):742-7 (medline /12574402)
COMMENTS: Cites: J Neurochem. 2003 Mar;84(6):1431-41 (medline /12614343)
COMMENTS: Cites: Cereb Cortex. 2003 Apr;13(4):400-8 (medline /12631569)
COMMENTS: Cites: Am J Psychiatry. 2003 Jun;160(6):1041-52 (medline /12777258)
COMMENTS: Cites: Behav Neurosci. 2003 Aug;117(4):728-37 (medline /12931958)
COMMENTS: Cites: Neuropsychopharmacology. 2004 Jan;29(1):81-5 (medline /12955098)
COMMENTS: Cites: Nat Neurosci. 2003 Nov;6(11):1208-15 (medline /14566342)
COMMENTS: Cites: Behav Neurosci. 2003 Oct;117(5):927-38 (medline /14570543)
COMMENTS: Cites: Eur J Neurosci. 2004 Jan;19(1):181-9 (medline /14750976)
COMMENTS: Cites: Eur J Neurosci. 2004 Apr;19(7):1997-2002 (medline /15078575)
COMMENTS: Cites: Science. 2004 Aug 13;305(5686):1017-9 (medline /15310907)
COMMENTS: Cites: J Neurosci. 2004 Aug 25;24(34):7482-90 (medline /15329395)
COMMENTS: Cites: Neurobiol Learn Mem. 2004 Sep;82(2):159-63 (medline /15341801)
COMMENTS: Cites: Neuron. 2004 Sep 30;44(1):161-79 (medline /15450168)
COMMENTS: Cites: Neuron. 2004 Dec 2;44(5):877-88 (medline /15572117)
COMMENTS: Cites: Science. 2004 Dec 10;306(5703):1944-7 (medline /15591205)
COMMENTS: Cites: Nat Neurosci. 2005 Feb;8(2):212-9 (medline /15657599)
COMMENTS: Cites: Neuron. 2005 Jun 16;46(6):933-43 (medline /15953421)
COMMENTS: Cites: Trends Neurosci. 2005 Aug;28(8):436-45 (medline /15982754)
COMMENTS: Cites: Biol Psychiatry. 2005 Sep 15;58(6):488-94 (medline /16023086)
COMMENTS: Cites: Eur J Neurosci. 2005 Jul;22(2):513-23 (medline /16045504)
COMMENTS: Cites: Neuron. 2005 Sep 15;47(6):873-84 (medline /16157281)
COMMENTS: Cites: J Neurochem. 2005 Dec;95(5):1481-94 (medline /16219028)
COMMENTS: Cites: Nat Neurosci. 2005 Nov;8(11):1481-9 (medline /16251991)
COMMENTS: Cites: Trends Cogn Sci. 2006 Feb;10(2):59-63 (medline /16406760)
COMMENTS: Cites: Nat Neurosci. 2006 Feb;9(2):167-9 (medline /16415868)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2932-7 (medline /16473939)
COMMENTS: Cites: Biol Psychiatry. 2006 Aug 15;60(4):352-60 (medline /16616731)
COMMENTS: Cites: Behav Brain Res. 2006 Sep 15;172(1):173-8 (medline /16769132)
COMMENTS: Cites: J Neurosci. 2006 Jun 14;26(24):6583-8 (medline /16775146)
COMMENTS: Cites: Annu Rev Neurosci. 2006;29:565-98 (medline /16776597)
COMMENTS: Cites: J Neurosci. 2006 Sep 6;26(36):9196-204 (medline /16957076)
COMMENTS: Cites: Eur J Neurosci. 2006 Sep;24(6):1733-43 (medline /17004937)
COMMENTS: Cites: Psychoneuroendocrinology. 2009 Apr;34(3):343-52 (medline /18977603)
COMMENTS: Cites: Ann N Y Acad Sci. 2008 Oct;1139:350-7 (medline /18991881)
COMMENTS: Cites: Nature. 2008 Nov 13;456(7219):245-9 (medline /19005555)
COMMENTS: Cites: J Exp Psychol Anim Behav Process. 1975 Oct;1(4):335-45 (medline /1202140)
COMMENTS: Cites: Brain Res. 1991 May 10;548(1-2):100-10 (medline /1651140)
COMMENTS: Cites: Science. 1989 Sep 29;245(4925):1511-3 (medline /2781295)
COMMENTS: Cites: J Comp Physiol Psychol. 1972 May;79(2):307-17 (medline /5025999)
COMMENTS: Cites: Biol Psychiatry. 2002 Jul 15;52(2):111-8 (medline /12114002)
COMMENTS: Cites: Neuron. 2002 Aug 15;35(4):605-23 (medline /12194863)
COMMENTS: Cites: Psychopharmacol Bull. 2001 Winter;35(1):84-94 (medline /12397873)
ABSTRACT: Over the past several years, drug addiction has increasingly been accepted to be a disease of the brain as opposed to simply being due to a lack of willpower or personality flaw. Exposure to addictive substances has been shown to create enduring changes in brain structure and function that are thought to underlie the transition to addiction. Specific genetic and environmental vulnerability factors also influence the impact of drugs of abuse on the brain and can enhance the likelihood of becoming an addict. Long-lasting alterations in brain function have been found in neural circuits that are known to be responsible for normal appetitive learning and memory processes and it has been hypothesized that drugs of abuse enhance positive learning and memory about the drug while inhibiting learning about the negative consequences of drug use. Therefore, the addict's behavior becomes increasingly directed towards obtaining and using drugs of abuse, while at the same time developing a poorer ability to stop using, even when the drug is less rewarding or interferes with functioning in other facets of life. In this review we will discuss the clinical evidence that addicted individuals have altered learning and memory and describe the possible neural substrates of this dysfunction. In addition, we will explore the pre-clinical evidence that drugs of abuse cause a progressive disorder of learning and memory, review the molecular and neurobiological changes that may underlie this disorder, determine the genetic and environmental factors that may increase vulnerability to addiction, and suggest potential strategies for treating addiction through manipulations of learning and memory.
MESH HEADINGS: Brain/*physiopathology
MESH HEADINGS: Humans
MESH HEADINGS: Learning/*physiology
MESH HEADINGS: Memory/*physiology
MESH HEADINGS: Reward
MESH HEADINGS: Substance-Related Disorders/*physiopathology/psychology eng

1389. Torres-Altoro, M. I.; Mathur, B. N.; Drerup, J. M.; Thomas, R.; Lovinger, D. M.; O'Callaghan, J. P., and Bibb, J. A. Organophosphates dysregulate dopamine signaling, glutamatergic neurotransmission, and induce neuronal injury markers in striatum. 2011; 119 , (2): 303-313.


Rec #: 70719
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: The neurological effects of organophosphate (OP) pesticides, commonly used on foods and in households, are an important public health concern. Furthermore, subclinical exposure to combinations of organophosphates is implicated in Gulf War illness. Here, we characterized the effects of the broadly used insecticide chlorpyrifos (CPF) on dopamine and glutamatergic neurotransmission effectors in corticostriatal motor/reward circuitry. CPF potentiated protein kinase A (PKA)-dependent phosphorylation of the striatal protein dopamine-and cAMP-regulated phosphoprotein of M(r) 32 kDa (DARPP-32) and the glutamate receptor 1 (GluR1) subunit of alpha-amino-3-hydroxy-5methyl- 4-isoxazolepropionic acid (AMPA) receptors in mouse brain slices. It also increased GluR1 phosphorylation by PKA when administered systemically. This correlated with enhanced glutamate release from cortical projections in rat striatum. Similar effects were induced by the sarin congener, diisopropyl fluorophosphate, alone or in combination with the putative neuroprotectant, pyridostigmine bromide and the pesticide N,N-diethyl-meta-toluamide (DEET). This combination, meant to mimic the neurotoxicant exposure encountered by veterans of the 1991 Persian Gulf War, also induced hyperphosphorylation of the neurofibrillary tangle-associated protein tau. Diisopropyl fluorophosphate and pyrodostigmine bromide, alone or in combination, also increased the aberrant activity of the protein kinase, Cdk5, as indicated by conversion of its activating cofactor p35 to p25. Thus, consistent with recent findings in humans and animals, organophosphate exposure causes dysregulation in the motor/reward circuitry and invokes mechanisms associated with neurological disorders and neurodegeneration.
Keywords: chlorpyrifos, dopamine, Gulf War illness, insecticide, neurotoxicity,
ISI Document Delivery No.: 834PE

1390. Tortella, G. R.; Rubilar, O.; Castillo, M. d. P.; Cea, M.; Mella-Herrera, R., and Diez, M. C. Chlorpyrifos degradation in a biomixture of biobed at different maturity stages . 2012 Jun; 88, (2): 224-228.


Rec #: 880
Keywords: FATE
Notes: Chemical of Concern: CPY
Abstract: The biomixture is a principal element controlling the degradation efficacy of the biobed. The maturity of the biomixture used in the biobed affects its overall performance of the biobed, but this is not well studied yet. The aim of this research was to evaluate the effect of using a typical composition of Swedish biomixture at different maturity stages on the degradation of chlorpyrifos. Tests were made using biomixture at three maturity stages: 0 d (BC0), 15 d (BC15) and 30 d (BC30); chlorpyrifos was added to the biobeds at final concentration of 200, 320 and 480 mg kgęĆ1. Chlorpyrifos degradation in the biomixture was monitored over time. Formation of TCP (3,5,6-trichloro-2-pyrinidol) was also quantified, and hydrolytic and phenoloxidase activities measured. The biomixture efficiently degraded chlorpyrifos (degradation efficiency >50%) in all the evaluated maturity stages. However, chlorpyrifos degradation decreased with increasing concentrations of the pesticide. TCP formation occurred in all biomixtures, but a major accumulation was observed in BC30. Significant differences were found in both phenoloxidase and hydrolytic activities in the three maturity stages of biomixture evaluated. Also, these two biological activities were affected by the increase in pesticide concentration. In conclusion, our results demonstrated that chlorpyrifos can be degraded efficiently in all the evaluated maturity stages. Biobeds/ Maturity stage/ Chlorpyrifos/ Biological activity

1391. Toutoudaki, M.; Kavvalakis, M.; Tzatzarakis, M.; Alegakis, A.; Dawson, A.; Fahim, M., and Tsatsakis, A. DEP and DETP concentration profiles along the hair shaft of two patients poisoned by chlorpyrifos: The use of hair analysis to confirm past acute exposure: Abstracts of the 47th Congress of the European Societies of Toxicology (EUROTOX). 2011 Aug 28-; 205, Supplement, (0): S70-S71.


Rec #: 2600
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY

1392. Trimble, A. J. Determining the Occurrence, Fate, and Effects of Pesticide Mixtures Using the Aquatic Amphipod Hyalella azteca. 2009: 198 p. (UMI #3372576).


Rec #: 360
Keywords: PUBL AS,SEDIMENT CONC
Call Number: NO PUBL AS (ATZ,BFT,CPY,CYF,CYP,DCT,DEATZ,DIATZ,DM,EFV,ES1,ES2,ESS,LCYT,PMR,PMT,PPZ,PRO,SZ), NO SEDIMENT CONC (ATZ,BFT,CPY,CYF,CYP,DCT,DEATZ,DIATZ,DM,EFV,ES1,ES2,ESS,LCYT,PMR,PMT,PPZ,PRO,SZ)
Notes: Chemical of Concern: AMTR,ATZ,BFT,CPY,CYF,CYP,CZE,DCT,DDE,DDT,DEATZ,DIATZ,DLD,DM,EFV,EN,ES1,ES2,ESS,HCCH,HPT,KCl,LCYT,MXC,PMR,PMT,PPCP,PPZ,PRO,SZ

1393. Trimble, A. J.; Weston, D. P.; Belden, J. B., and Lydy, M. J. Identification and Evaluation of Pyrethroid Insecticide Mixtures in Urban Sediments. 2009; 28, (8): 1687-1695.


Rec #: 1510
Keywords: MIXTURE,REFS CHECKED,REVIEW
Call Number: NO MIXTURE (BFT,CPY,CYF,CYP,DM,EFV,ES1,ES2,ESS,LCYT,PMR), NO REFS CHECKED (BFT,CPY,CYF,CYP,DM,EFV,ES1,ES2,ESS,LCYT,PMR), NO REVIEW (BFT,CPY,CYF,CYP,DM,EFV,ES1,ES2,ESS,LCYT,PMR)
Notes: Chemical of Concern: BFT,CPY,CYF,CYP,DDT,DLD,DM,EFV,EN,ES1,ES2,ESS,LCYT,MXC,PMR

1394. Trivedi, N. N. and Caughey, G. H. Mast Cell Peptidases: Chameleons of Innate Immunity and Host Defense.


Rec #: 50649
Keywords: NO TOXICANT
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: J Biol Chem. 2006 Jan 20;281(3):1489-94 (medline /16303761)
COMMENTS: Cites: Dev Comp Immunol. 2006;30(10):901-18 (medline /16413608)
COMMENTS: Cites: J Mol Biol. 2006 Mar 17;357(1):195-209 (medline /16414069)
COMMENTS: Cites: FEBS J. 2006 May;273(9):1871-95 (medline /16640553)
COMMENTS: Cites: J Allergy Clin Immunol. 2006 Jun;117(6):1411-4 (medline /16751005)
COMMENTS: Cites: Immunogenetics. 2006 Aug;58(8):655-69 (medline /16807745)
COMMENTS: Cites: Immunogenetics. 2006 Aug;58(8):641-54 (medline /16807746)
COMMENTS: Cites: Pharmacol Ther. 2006 Dec;112(3):668-76 (medline /16837049)
COMMENTS: Cites: Science. 2006 Jul 28;313(5786):526-30 (medline /16873664)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2007 Feb 13;104(7):2325-30 (medline /17277081)
COMMENTS: Cites: Am J Pathol. 2007 Mar;170(3):930-40 (medline /17322378)
COMMENTS: Cites: Clin Immunol. 2007 Jun;123(3):268-71 (medline /17449330)
COMMENTS: Cites: J Biol Chem. 2007 Jul 20;282(29):20809-15 (medline /17456473)
COMMENTS: Cites: Immunol Rev. 2007 Jun;217:141-54 (medline /17498057)
COMMENTS: Cites: J Biol Chem. 2007 Jul 20;282(29):20785-9 (medline /17504754)
COMMENTS: Cites: Gastroenterology. 2007 Jun;132(7):2422-37 (medline /17570216)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15858-63 (medline /17898169)
COMMENTS: Cites: J Exp Med. 2007 Oct 29;204(11):2629-39 (medline /17923505)
COMMENTS: Cites: J Immunol. 2007 Nov 1;179(9):6072-9 (medline /17947681)
COMMENTS: Cites: Arthritis Rheum. 2007 Nov;56(11):3532-40 (medline /17968878)
COMMENTS: Cites: J Biol Chem. 2008 Jan 4;283(1):427-36 (medline /17981788)
COMMENTS: Cites: Genes Dev. 1999 Jun 1;13(11):1382-97 (medline /10364156)
COMMENTS: Cites: J Biol Chem. 1999 Jul 9;274(28):19670-6 (medline /10391906)
COMMENTS: Cites: Clin Exp Allergy. 2002 Jul;32(7):1000-6 (medline /12100045)
COMMENTS: Cites: Clin Exp Allergy. 2003 Jul;33(7):1005-12 (medline /12859460)
COMMENTS: Cites: J Med Chem. 2003 Aug 28;46(18):3865-76 (medline /12930148)
COMMENTS: Cites: J Histochem Cytochem. 1953 Nov;1(6):469-70 (medline /13118129)
COMMENTS: Cites: Ann N Y Acad Sci. 1963 Feb 26;103:185-98 (medline /13928097)
COMMENTS: Cites: Biol Chem. 2003 Oct-Nov;384(10-11):1527-31 (medline /14669996)
COMMENTS: Cites: J Pharmacol Exp Ther. 2004 Apr;309(1):119-26 (medline /14722328)
COMMENTS: Cites: J Immunol. 1992 Apr 15;148(8):2475-82 (medline /1560203)
COMMENTS: Cites: Arch Biochem Biophys. 2005 Mar 15;435(2):311-22 (medline /15708374)
COMMENTS: Cites: J Histochem Cytochem. 1992 Jun;40(6):781-6 (medline /1588024)
COMMENTS: Cites: J Pathol. 2005 Jul;206(3):279-90 (medline /15887294)
COMMENTS: Cites: Am J Respir Cell Mol Biol. 1990 Jul;3(1):27-32 (medline /1694672)
COMMENTS: Cites: J Med Chem. 2007 Apr 19;50(8):1727-30 (medline /17361995)
COMMENTS: Cites: J Clin Invest. 1991 Aug;88(2):493-9 (medline /1864960)
COMMENTS: Cites: J Clin Invest. 1990 Mar;85(3):682-9 (medline /2107207)
COMMENTS: Cites: Am J Respir Cell Mol Biol. 1990 May;2(5):449-52 (medline /2187492)
COMMENTS: Cites: J Immunol. 1990 Oct 15;145(8):2652-61 (medline /2212656)
COMMENTS: Cites: J Immunol. 1987 Oct 15;139(8):2724-9 (medline /2443571)
COMMENTS: Cites: J Pharmacol Exp Ther. 1988 Jan;244(1):133-7 (medline /2447273)
COMMENTS: Cites: J Pharmacol Exp Ther. 1989 Mar;248(3):947-51 (medline /2495355)
COMMENTS: Cites: Biochemistry. 1989 May 16;28(10):4148-55 (medline /2504277)
COMMENTS: Cites: Bioorg Med Chem Lett. 1999 Aug 2;9(15):2199-204 (medline /10465545)
COMMENTS: Cites: Biochem Pharmacol. 1999 Dec 15;58(12):1989-96 (medline /10591155)
COMMENTS: Cites: J Med Genet. 1999 Dec;36(12):881-7 (medline /10593994)
COMMENTS: Cites: Am J Respir Cell Mol Biol. 2000 Feb;22(2):183-90 (medline /10657939)
COMMENTS: Cites: Immunity. 2000 Feb;12(2):201-10 (medline /10714686)
COMMENTS: Cites: J Exp Med. 2000 Dec 18;192(12):1849-56 (medline /11120781)
COMMENTS: Cites: J Biol Chem. 2001 May 25;276(21):18551-6 (medline /11279033)
COMMENTS: Cites: J Biol Chem. 2001 Jul 13;276(28):26276-84 (medline /11335723)
COMMENTS: Cites: J Allergy Clin Immunol. 2001 Jun;107(6):1039-45 (medline /11398082)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7469-74 (medline /11416217)
COMMENTS: Cites: Am J Respir Crit Care Med. 2001 Oct 1;164(7):1276-81 (medline /11673222)
COMMENTS: Cites: J Immunol. 2002 Feb 15;168(4):1992-2000 (medline /11823536)
COMMENTS: Cites: J Clin Invest. 2002 Feb;109(3):363-71 (medline /11827996)
COMMENTS: Cites: Aliment Pharmacol Ther. 2002 Mar;16(3):407-13 (medline /11876693)
COMMENTS: Cites: N Engl J Med. 2002 May 30;346(22):1699-705 (medline /12037149)
COMMENTS: Cites: Science. 2002 Sep 6;297(5587):1689-92 (medline /12215644)
COMMENTS: Cites: Mol Immunol. 2002 Sep;38(16-18):1353-7 (medline /12217407)
COMMENTS: Cites: Bioorg Med Chem Lett. 2002 Nov 4;12(21):3229-33 (medline /12372540)
COMMENTS: Cites: J Immunol. 2002 Nov 1;169(9):5145-52 (medline /12391231)
COMMENTS: Cites: J Biol Chem. 2003 Jan 31;278(5):3363-71 (medline /12441343)
COMMENTS: Cites: Eur J Biochem. 2002 Dec;269(23):5921-30 (medline /12444981)
COMMENTS: Cites: Biochemistry. 2003 Mar 11;42(9):2616-24 (medline /12614156)
COMMENTS: Cites: J Biol Chem. 2003 Sep 5;278(36):34517-24 (medline /12815038)
COMMENTS: Cites: Nat Rev Genet. 2003 Jul;4(7):544-58 (medline /12838346)
COMMENTS: Cites: J Neurosci. 2003 Jul 16;23(15):6176-80 (medline /12867500)
COMMENTS: Cites: J Biol Chem. 2003 Oct 10;278(41):39625-31 (medline /12900423)
COMMENTS: Cites: J Exp Med. 2003 Aug 4;198(3):423-31 (medline /12900518)
COMMENTS: Cites: Am J Respir Cell Mol Biol. 2004 Apr;30(4):519-29 (medline /12959947)
COMMENTS: Cites: J Exp Med. 1959 Sep 1;110:451-60 (medline /13798801)
COMMENTS: Cites: J Biol Chem. 2004 Jan 23;279(4):2438-52 (medline /14583634)
COMMENTS: Cites: J Clin Invest. 2004 Feb;113(4):628-34 (medline /14966572)
COMMENTS: Cites: Genome Res. 2004 Apr;14(4):609-22 (medline /15060002)
COMMENTS: Cites: J Biol Chem. 2004 Jul 30;279(31):32339-44 (medline /15173164)
COMMENTS: Cites: Eur J Pharmacol. 2004 Jun 16;493(1-3):173-6 (medline /15189779)
COMMENTS: Cites: Nature. 2004 Nov 25;432(7016):512-6 (medline /15543132)
COMMENTS: Cites: Am J Respir Crit Care Med. 2005 Mar 1;171(5):431-9 (medline /15563633)
COMMENTS: Cites: J Immunol. 2004 Dec 15;173(12):7277-81 (medline /15585850)
COMMENTS: Cites: J Biol Chem. 2005 Mar 11;280(10):9291-6 (medline /15615702)
COMMENTS: Cites: J Biol Chem. 2005 May 6;280(18):18001-7 (medline /15741158)
COMMENTS: Cites: J Immunol. 2005 Jun 1;174(11):7285-91 (medline /15905575)
COMMENTS: Cites: Immunity. 2005 Jun;22(6):679-91 (medline /15963783)
COMMENTS: Cites: Biochemistry (Mosc). 2005 Jun;70(6):672-84 (medline /16038610)
COMMENTS: Cites: J Immunol. 2005 Aug 15;175(4):2635-42 (medline /16081839)
COMMENTS: Cites: J Histochem Cytochem. 1989 Oct;37(10):1509-15 (medline /2674273)
COMMENTS: Cites: Arch Biochem Biophys. 1987 Nov 1;258(2):555-63 (medline /3118812)
COMMENTS: Cites: J Histochem Cytochem. 1988 Aug;36(8):1053-60 (medline /3134486)
COMMENTS: Cites: N Engl J Med. 1987 Jun 25;316(26):1622-6 (medline /3295549)
COMMENTS: Cites: J Immunol. 1987 Apr 1;138(7):2184-9 (medline /3549898)
COMMENTS: Cites: Ann Rheum Dis. 1973 Nov;32(6):515-23 (medline /4543387)
COMMENTS: Cites: Ann Rheum Dis. 1971 Jan;30(1):24-30 (medline /5554508)
COMMENTS: Cites: Biochemistry. 1978 Mar 7;17(5):811-9 (medline /629933)
COMMENTS: Cites: J Biol Chem. 1983 Nov 25;258(22):13552-7 (medline /6358206)
COMMENTS: Cites: J Biol Chem. 1984 Sep 10;259(17):11046-51 (medline /6432791)
COMMENTS: Cites: Arthritis Rheum. 1984 Aug;27(8):845-51 (medline /6466393)
COMMENTS: Cites: J Biol Chem. 1982 Aug 10;257(15):8619-22 (medline /6807977)
COMMENTS: Cites: J Biol Chem. 1981 Nov 25;256(22):11939-43 (medline /7028744)
COMMENTS: Cites: J Immunol. 1995 May 15;154(10):5472-80 (medline /7730649)
COMMENTS: Cites: Biol Chem Hoppe Seyler. 1994 Oct;375(10):685-94 (medline /7888081)
COMMENTS: Cites: J Pharmacol Exp Ther. 1993 Feb;264(2):676-82 (medline /8437115)
COMMENTS: Cites: Am J Respir Crit Care Med. 1995 Dec;152(6 Pt 1):2076-83 (medline /8520778)
COMMENTS: Cites: J Immunol. 1996 Jan 1;156(1):275-83 (medline /8598474)
COMMENTS: Cites: J Immunol. 1997 Dec 15;159(12):6216-25 (medline /9550425)
COMMENTS: Cites: Biochim Biophys Acta. 1998 Jul 28;1386(1):189-98 (medline /9675278)
COMMENTS: Cites: J Biol Chem. 1999 Feb 5;274(6):3355-62 (medline /9920877)
COMMENTS: Cites: Mol Immunol. 2008 Apr;45(7):2116-25 (medline /18022236)
COMMENTS: Cites: J Allergy Clin Immunol. 2008 May;121(5):1262-8 (medline /18325577)
COMMENTS: Cites: J Biol Chem. 2008 May 16;283(20):13943-51 (medline /18353771)
COMMENTS: Cites: J Immunol. 2008 Apr 1;180(7):4885-91 (medline /18354212)
COMMENTS: Cites: Nat Med. 2008 Apr;14(4):392-8 (medline /18376408)
COMMENTS: Cites: Arthritis Rheum. 2008 Aug;58(8):2338-46 (medline /18668540)
COMMENTS: Cites: J Immunol. 2008 Oct 15;181(8):5598-605 (medline /18832718)
COMMENTS: Cites: J Biol Chem. 2008 Dec 5;283(49):34178-87 (medline /18854315)
COMMENTS: Cites: Eur J Immunol. 2009 Jan;39(1):11-25 (medline /19130582)
COMMENTS: Cites: Thorax. 2009 Apr;64(4):297-305 (medline /19131451)
COMMENTS: Cites: J Immunol. 2009 May 1;182(9):5770-7 (medline /19380825)
COMMENTS: Cites: Nat Med. 2009 Aug;15(8):940-5 (medline /19633655)
COMMENTS: Cites: Clin Exp Allergy. 2009 Oct;39(10):1450-2 (medline /19678824)
COMMENTS: Cites: J Allergy Clin Immunol. 2009 Nov;124(5):1099-105.e1-4 (medline /19748655)
COMMENTS: Cites: J Immunol. 1991 Jul 1;147(1):247-53 (medline /2051021)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1989 Dec;86(23):9480-4 (medline /2594780)
COMMENTS: Cites: J Clin Invest. 1989 Jan;83(1):175-9 (medline /2642918)
COMMENTS: Cites: Biochemistry. 1985 Apr 9;24(8):2048-58 (medline /3893542)
COMMENTS: Cites: Am J Respir Cell Mol Biol. 1995 Aug;13(2):227-36 (medline /7626290)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1994 Jan 4;91(1):128-32 (medline /8278352)
COMMENTS: Cites: J Immunol. 1993 Sep 1;151(5):2699-706 (medline /8360486)
COMMENTS: Cites: Genomics. 1993 Mar;15(3):614-20 (medline /8468056)
COMMENTS: Cites: Nature. 1996 May 2;381(6577):75-7 (medline /8609992)
COMMENTS: Cites: Nature. 1996 May 2;381(6577):77-80 (medline /8609993)
COMMENTS: Cites: J Clin Invest. 1996 Feb 15;97(4):988-95 (medline /8613553)
COMMENTS: Cites: Am J Respir Crit Care Med. 1996 Sep;154(3 Pt 1):649-53 (medline /8810600)
COMMENTS: Cites: EMBO J. 1996 Oct 15;15(20):5481-91 (medline /8896442)
COMMENTS: Cites: Eur Respir J. 1997 Jan;10(1):38-43 (medline /9032489)
COMMENTS: Cites: J Clin Invest. 1997 Sep 15;100(6):1383-93 (medline /9294103)
COMMENTS: Cites: J Biol Chem. 1997 Oct 10;272(41):25628-35 (medline /9325284)
COMMENTS: Cites: J Immunol. 1998 Feb 15;160(4):1910-9 (medline /9469453)
COMMENTS: Cites: Nature. 1998 Mar 19;392(6673):306-11 (medline /9521329)
COMMENTS: Cites: J Biol Chem. 1998 Jun 19;273(25):15514-20 (medline /9624139)
COMMENTS: Cites: J Mol Biol. 1999 Feb 12;286(1):163-73 (medline /9931257)
COMMENTS: Cites: J Immunol. 2000 Jun 15;164(12):6566-75 (medline /10843716)
COMMENTS: Cites: Biochim Biophys Acta. 2000 Jul 14;1480(1-2):245-57 (medline /10899625)
COMMENTS: Cites: Bioorg Med Chem Lett. 2000 Oct 16;10(20):2361-6 (medline /11055356)
COMMENTS: Cites: J Immunol. 2001 Feb 15;166(4):2783-92 (medline /11160345)
COMMENTS: Cites: Bioorg Med Chem. 2001 Feb;9(2):301-15 (medline /11249123)
COMMENTS: Cites: Bioorg Med Chem. 2001 Nov;9(11):3065-75 (medline /11597491)
COMMENTS: Cites: EMBO J. 2001 Dec 3;20(23):6570-82 (medline /11726493)
COMMENTS: Cites: J Immunol. 2002 Jan 1;168(1):290-7 (medline /11751973)
COMMENTS: Cites: Biochim Biophys Acta. 2002 Apr 29;1596(2):346-56 (medline /12007614)
COMMENTS: Comment in: Am J Respir Cell Mol Biol. 2010 Mar;42(3):255-6 (medline /20156978)
ABSTRACT: Mast cells make and secrete an abundance of peptidases, which are stored in such large amounts in granules that they comprise a high fraction of all cellular protein. Perhaps no other immune cell is so generously endowed with peptidases. For many years after the main peptidases were first described, they were best known as markers of degranulation, for they are released locally in response to mast cell stimulation and can be distributed systemically and detected in blood. The principal peptidases are tryptases, chymases, carboxypeptidase A3, and dipeptidylpeptidase I (cathepsin C). Numerous studies suggest that these enzymes are important and even critical for host defense and homeostasis. Endogenous and allergen or pathogen-associated targets have been identified. Belying the narrow notion of peptidases as proinflammatory, several of the peptidases limit inflammation and toxicity of endogenous peptides and venoms. The peptidases are interdependent, so that absence or inactivity of one enzyme can alter levels and activity of others. Mammalian mast cell peptidases--chymases and tryptases especially--vary remarkably in number, expression, biophysical properties, and specificity, perhaps because they hyper-evolved under pressure from the very pathogens they help to repel. Tryptase and chymase involvement in some pathologies stimulated development of therapeutic inhibitors for use in asthma, lung fibrosis, pulmonary hypertension, ulcerative colitis, and cardiovascular diseases. While animal studies support the potential for mast cell peptidase inhibitors to mitigate certain diseases, other studies, as in mice lacking selected peptidases, predict roles in defense against bacteria and parasites and that systemic inactivation may impair host defense.
MESH HEADINGS: Animals
MESH HEADINGS: Host-Pathogen Interactions/*immunology
MESH HEADINGS: Humans
MESH HEADINGS: Immunity, Innate/*immunology
MESH HEADINGS: Mast Cells/*enzymology/*immunology
MESH HEADINGS: Peptide Hydrolases/*immunology eng

1395. Tsiplakou, E; Anagnostopoulos, C J; Liapis, K; Haroutounian, Sa; Zervas, G, and Tsiplakou, E. Pesticides Residues in Milks and Feedstuff of Farm Animals Drawn From Greece. 2010 Jul; 80, (5): 504-512.


Rec #: 47839
Keywords: FOOD
Notes: Chemical of Concern: CPY
Abstract: Abstract: The objective of this study was to investigate if milk from dairy sheep and goats, fed mainly with supplementary feed during the winter months, was contaminated with pesticides residues. Two hundred milk samples from sheep and goats were collected from 10 farms of each animals. The sheep and goats farms were selected from those which represent common conventional production and feeding systems in Greece. Milk and feed samples (alfalfa hay, wheat straw, shrubs, pasture and concentrates) were taken from each farm to analyze for pesticides residues. The results showed that the capital sigma endosulfan was the main pesticide residue which was detected in all the concentrates samples at a mean concentration of 5.36 mg kg super(-1), which is much higher from the maximum residue level (MRL). In addition, the capital sigma endosulfan was also detected in all the alfalfa hay samples but at a mean concentration of 0.10 mg kg super(-1) which is lower than the MRL. The mean concentrations of endosulfan alpha and beta were 2.82 and 2.39 mg kg super(-1) in the concentrates samples and 0.08 and 0.02 mg kg super(-1) respectively in alfalfa hay samples. In the wheat straw, shrubs and pasture samples no pesticides residues were detected. No pesticide residues were also detected in milk samples of sheep and goats. Thus, this milk from the farms sampled presents no human health risks as far as the contaminants analyzed concerned.
Keywords: wheat
Keywords: Milk
Keywords: Greece
Keywords: Feed
Keywords: Pesticide residues
Keywords: alfalfa
Keywords: Q5 01502:Methods and instruments
Keywords: P 6000:TOXICOLOGY AND HEALTH
Keywords: Pasture
Keywords: ENA 02:Toxicology & Environmental Safety
Keywords: Environmental Studies
Keywords: Public health
Keywords: Feed composition
Keywords: Triticum aestivum
Keywords: farms
Keywords: Pesticides
Keywords: hay
Keywords: Environment Abstracts; Pollution Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality
Keywords: sheep
Keywords: Feeds
Date revised - 2011-10-01
Language of summary - English
Location - Greece
Pages - 504-512
ProQuest ID - 813723319
SubjectsTermNotLitGenreText - Feed; Pesticides; Feed composition; Public health; wheat; Milk; Pesticide residues; farms; hay; alfalfa; sheep; Pasture; Feeds; Triticum aestivum; Greece
Last updated - 2011-12-07
Corporate institution author - Tsiplakou, E; Anagnostopoulos, C J; Liapis, K; Haroutounian, SA; Zervas, G
DOI - OB-ee8e5764-d1a2-481a-8ffdcsaobj202; 13146528; CS1115603; 0045-6535 English

1396. Tulve, N. S.; Egeghy, P. P.; Fortmann, R. C.; Xue, J. P.; Evans, J.; Whitaker, D. A., and Croghan, C. W. Methodologies for estimating cumulative human exposures to current-use pyrethroid pesticides. 2011; 21, (3): 317-327.


Rec #: 70839
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: We estimated cumulative residential pesticide exposures for a group of nine young children (4-6 years) using three different methodologies developed by the US Environmental Protection Agency and compared the results with estimates derived from measured urinary metabolite concentrations. The Standard Operating Procedures (SOPs) for Residential Exposure Assessment are intended to provide a screening-level assessment to estimate exposure for regulatory purposes. Nonetheless, dermal exposure estimates were typically lower from the SOP (1-1300 nmol/day) than from SHEDS (5-19,000 nmol/day) or any of the four different approaches for estimating dermal exposure using the Draft Protocol for Measuring Children's Non-Occupational Exposure to Pesticides by all Relevant Pathways (Draft Protocol) (5-11,000 nmol/day). Indirect ingestion exposure estimates ranged from 0.02 to 21.5 nmol/day for the SOP, 0.5 to 188 nmol/day for SHEDS, and 0 to 3.38 nmol/day for the Draft Protocol. Estimates of total absorbed dose ranged from 3 to 37 nmol/day for the SOPs, 0.5 to 100 nmol/day for SHEDS, and 1 to 216 nmol/day for the Draft Protocol. The concentrations estimated using the Draft Protocol and SHEDS showed strong, positive relationships with the 3-phenoxybenzoic acid metabolite measured in the children's urine samples (R(2) = 0.90 for the Draft Protocol; R(2) = 0.92 for SHEDS). Analysis of different approaches for estimating dermal exposure suggested that the approach assuming an even distribution of pesticide residue on the child's body was most reasonable. With all three methodologies providing reasonable estimates of exposure and dose, selection should depend on the available data and the objectives of the analysis. Further research would be useful to better understand how best to estimate dermal exposure for children and what exposure factors (e.g., activities, transfer coefficients, measurement techniques) are most relevant in making dermal exposure estimates. Journal of Exposure Science and Environmental Epidemiology (2011) 21, 317-327; doi:10.1038/jes.2010.25; published online 21 April 2010
Keywords: cumulative exposure, dermal, indirect ingestion, diet, inhalation,
ISI Document Delivery No.: 752RY

1397. Turci, R.; Sturchio, E.; Businaro, J.; Casorri, L.; Imbriani, M., and Minoia, C. [The Endocrine Disruptors. Monographies. 6. Chlorpyrifos and Chlorpyrifos-Methyl].


Rec #: 75279
Keywords: NON-ENGLISH
Notes: Chemical of Concern: CPY
Abstract: MESH HEADINGS: Animals
MESH HEADINGS: Chlorpyrifos/analogs &
MESH HEADINGS: derivatives/chemistry/*toxicity/urine
MESH HEADINGS: Endocrine Disruptors/chemistry/*toxicity/urine
MESH HEADINGS: *Environmental Monitoring/legislation &
MESH HEADINGS: jurisprudence/methods
MESH HEADINGS: Evidence-Based Medicine
MESH HEADINGS: Humans
MESH HEADINGS: Insecticides/chemistry/*toxicity/urine
MESH HEADINGS: Occupational Exposure/*adverse effects/legislation &
MESH HEADINGS: jurisprudence
MESH HEADINGS: Risk Assessment
MESH HEADINGS: Risk Factors ita. Interferenti i endocrini--Schede monografiche. 6. Clorpirifos e clorpirifos-metile.

1398. Turgut, C.; Ornek, H., and Cutright, T. J. Determination of pesticide residues in Turkey's table grapes: the effect of integrated pest management, organic farming, and conventional farming. 2011; 173, (1-4): 315-323.


Rec #: 70899
Keywords: SURVEY
Notes: Chemical of Concern: CPY
Abstract: Abstract: Turkey is one of the world's largest producers and exporters of table grapes. Growing social concerns over excessive pesticide use have led to farming to move from conventional to organic practices. Table grapes were collected from 99 different farms in three Aegean regions. Pesticide residues were only detected in farms using conventional agriculture practices while no pesticides were detected in grapes from farms using organic or integrated pest management. A risk assessment model indicated that lambda-cyhalothrin posed the most significant risk at conventional farms.
Keywords: Pesticide residues, Table grapes, Organic farming, IPM, Conventional
ISI Document Delivery No.: 729VY

1399. Turgut, Cafer; Ornek, Hakan, and Cutright, Teresa J. Pesticide Residues in Dried Table Grapes From the Aegean Region of Turkey. 2010 Aug; 167, (1-4): 143-9.


Rec #: 43959
Keywords: FOOD
Notes: Chemical of Concern: CPY
Abstract: Abstract: Issue Title: Special Issue: Environmental monitoring of offshore drilling for petroleum exploration (MAPEM Project): shallow waters / Guest Edited by SĂ©rgio A. Netto and Elirio E. Toldo Jr Dried grapes make the ideal low-calorie snack. The formation of gray mold during the drying of the grapes can severely decrease production. Pesticides and fungicides are applied to prevent losses due to pests and mold. Dried grapes from 99 farms in the Aegean region were sampled for pesticide residues. Of the 26 pesticides analyzed for, chlorpyrifos methyl, chlorpyrifos ethyl, deltamethrin, lambda-cyolathrin, dichlofluanid, iprodione, and procymidone were detected in the dried grapes. Only seven samples contained residues above the maximum residue limit. It is important to note that pesticide residues were only present in samples originating from vineyards using conventional farming practices.[PUBLICATION ABSTRACT]
Keywords: 8640:Chemical industry
Keywords: decamethrin
Keywords: dichlofluanid
Keywords: Bicyclo Compounds -- analysis
Keywords: 2600:Management science/operations research
Keywords: Environmental Studies
Keywords: 1540:Pollution control
Keywords: Chlorpyrifos -- analysis
Keywords: procymidone
Keywords: Pyrethrins -- analysis
Keywords: chlorpyrifos-methyl
Keywords: Vitis -- chemistry
Keywords: Nitriles -- analysis
Keywords: Aniline Compounds -- analysis
Keywords: Organothiophosphorus Compounds -- analysis
Keywords: Organothiophosphorus Compounds
Keywords: Food Contamination -- analysis
Keywords: Aniline Compounds
Keywords: Pesticide Residues
Keywords: Turkey
Keywords: 9130:Experimental/theoretical
Keywords: Chlorpyrifos
Keywords: Nitriles
Keywords: 8400:Agriculture industry
Keywords: Pyrethrins
Keywords: chlorpyrifos-ethyl
Keywords: Chlorpyrifos -- analogs & derivatives
Keywords: Pesticide Residues -- analysis
Keywords: Bicyclo Compounds
Copyright - Springer Science+Business Media B.V. 2010
Language of summary - English
Pages - 143-9
ProQuest ID - 609969247
Last updated - 2012-03-05
Place of publication - Dordrecht
Corporate institution author - Turgut, Cafer; Ornek, Hakan; Cutright, Teresa J
DOI - 2080632361; 53343771; 108264; EVMT; 19533395; SPVLEVMT106611671-41037 English

1400. U.S. Environmental Protection Agency. Methods for Measuring the Toxicity and Bioaccumulation of Sediment-Associated Contaminants with Freshwater Invertebrates. 1994: 133 p.


Rec #: 2400
Keywords: METHODS
Call Number: NO METHODS (CPY,Cu,CuS,HCL,MOL,Zn,Zn element)
Notes: Chemical of Concern: 1Major ions,CF,CPY,Cu,CuS,DDE,DDT,DLD,FML,HCL,KCl,MOL,Zn

1401. Uygun, Umran; Senoz, Berrin; Oeztuerk, Serpil; Koksel, Hamit, and Uygun, Umran. Degradation of Organophosphorus Pesticides in Wheat During Cookie Processing. 2009 Nov; 117 , (2): 261-264.


Rec #: 44559
Keywords: FOOD
Notes: Chemical of Concern: CPY
Abstract: Abstract: For investigating carryover of some organophosphorus pesticide residues in the cereal food chain from grain to consumer, a study was set up on wheat bran, flour and cookies, with and without bran. Special emphasis was given to malathion and chlorpyrifos-methyl residues in cookies for better protection of consumers. Pesticide-free wheat was placed in a small-scale model of a commercial storage vessel and treated with these pesticides. The residue levels of insecticides were determined in wheat, as well as in bran, flour and cookies produced from stored wheat at various time intervals during storage. A multiresidue analysis was performed using GC-NPD and GC-MS. Malathion and chlorpyrifos-methyl residue levels were higher than the maximum residue limits (MRLs) in wheat after 240 days of storage. MRLs established by the EC for malathion and chlorpyrifos-methyl in wheat are 8 and 3 mg kg super(-1), respectively. The residue levels of insecticides in flour samples also exceeded the MRL (2 mg kg super(-1) for both insecticides). Eight months of storage were not effective for reducing the residues in wheat to the levels below MRLs. Although, considerable amounts of the insecticides remained in the bran and flour, the cookie processing significantly reduced the concentrations in general. Chlorpyrifos-methyl was more persistent than was malathion and comparatively less degradation occurred during milling and cookie processing due to its physicochemical properties.
Keywords: Food processing
Keywords: Pesticides (organophosphorus)
Keywords: Food chains
Keywords: Physicochemical properties
Keywords: Malathion
Keywords: Models
Keywords: Triticum aestivum
Keywords: Insecticides
Keywords: Cereals
Keywords: Grain
Keywords: Consumers
Keywords: X 24330:Agrochemicals
Keywords: Toxicology Abstracts
Keywords: Flour
Date revised - 2009-07-01
Language of summary - English
Pages - 261-264
ProQuest ID - 20681591
SubjectsTermNotLitGenreText - Food processing; Pesticides (organophosphorus); Food chains; Insecticides; Cereals; Physicochemical properties; Grain; Consumers; Flour; Malathion; Models; Triticum aestivum
Last updated - 2013-02-08
British nursing index edition - Food Chemistry [Food Chem.]. Vol. 117, no. 2, pp. 261-264. Nov 2009.
Corporate institution author - Uygun, Umran; Senoz, Berrin; Oeztuerk, Serpil; Koksel, Hamit
DOI - MD-0009882199; 9454778; 0308-8146 English

1402. Valbonesi, P.; Brunelli, F.; Mattioli, M.; Rossi, T., and Fabbri, E. Cholinesterase Activities and Sensitivity to Pesticides in Different Tissues of Silver European Eel, Anguilla anguilla. University of Bologna, Interdepartmental Research Centre in Environmental Sciences, Laboratory of Environmental Physiology and Biochemistry, 163 via Sant'Alberto, I-48123, Ravenna, Italy.//: 2011; 154, (4): 353-359.


Rec #: 2200
Keywords: IN VITRO
Call Number: NO IN VITRO (CBF,CBL,CPY,DZ)
Notes: Chemical of Concern: CBF,CBL,CPY,DZ

1403. Valcke, M. and Bouchard, M. Determination of no-observed effect level (NOEL)-biomarker equivalents to interpret biomonitoring data for organophosphorus pesticides in children. 2009; 8, 5-5.


Rec #: 70979
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: Background: Environmental exposure to organophosphorus pesticides has been characterized in various populations, but interpretation of these data from a health risk perspective remains an issue. The current paper proposes biological reference values to help interpret biomonitoring data related to an exposure to organophosphorus pesticides in children for which measurements of alkylphosphate metabolites are available. Methods: Published models describing the kinetics of malathion and chlorpyrifos in humans were used to determine no-observed effect level - biomarker equivalents for methylphosphates and ethylphosphates, respectively. These were expressed in the form of cumulative urinary amounts of alkylphosphates over specified time periods corresponding to an absorbed no-observed effect level dose (derived from a published human exposure dose) and assuming various plausible exposure scenarios. Cumulative amounts of methylphosphate and ethylphosphate metabolites measured in the urine of a group of Quebec children were then compared to the proposed biological reference values. Results: From a published no-observed effect level dose for malathion and chlorpyrifos, the model predicts corresponding oral biological reference values for methylphosphate and ethylphosphate derivatives of 106 and 52 nmol/kg of body weight, respectively, in 12-h nighttime urine collections, and dermal biological reference values of 40 and 32 nmol/kg of body weight. Out of the 442 available urine samples, only one presented a methylphosphate excretion exceeding the biological reference value established on the basis of a dermal exposure scenario and none of the methylphosphate and ethylphosphate excretion values were above the obtained oral biological reference values, which reflect the main exposure route in children. Conclusion: This study is a first step towards the development of biological guidelines for organophophorus pesticides using a toxicokinetic modeling approach, which can be used to provide a health-based interpretation of biomonitoring data in the general population.
Keywords: BIOLOGICAL REFERENCE VALUES, PRESCHOOL-CHILDREN, WASHINGTON-STATE,
ISI Document Delivery No.: 422BD

1404. Valencia, T. M. G. and de Llasera, M. P. G. Determination of organophosphorus pesticides in bovine tissue by an on-line coupled matrix solid-phase dispersion-solid phase extraction-high performance liquid chromatography with diode array detection method. 2011; 1218, (39): 6869-6877.


Rec #: 70989
Keywords: CHEM METHODS
Notes: Chemical of Concern: CPY
Abstract: Abstract: A miniaturized method based on matrix solid-phase dispersion coupled to solid phase extraction and high performance liquid chromatography with diode array detection (MSPD-SPE-HPLC/DAD) was developed for the trace simultaneous determination of the following organophosphorus pesticides (OPPs) in bovine tissue: parathion-methyl, fenitrothion, parathion, chlorfenvinphos, diazinon, ethion, fenchlorphos, chlorpyrifos and carbophenothion. To perform the coupling between MSPD and SPE, 0.05 g of sample was dispersed with 0.2 g of C(18) silica sorbent and packed into a stainless steel cartridge containing 0.05 g of silica gel in the bottom. After a clean-up of high and medium polarity interferences with water and an acetonitrile:water mixture, the OPPs were desorbed from the MSPD cartridge with pure acetonitrile and directly transferred to a dynamic mixing chamber for dilution with water and preconcentration into an SPE 20 mm x 2.0 mm I.D. C(18) silica column. Subsequently, the OPPs were eluted on-line with the chromatographic mobile phase to the analytical column and the diode array detector for their separation and detection, respectively. The method was validated and yielded recovery values between 91% and 101% and precision values, expressed as relative standard deviations (RSD), which were less than or equal to 12%. Linearity was good and ranged from 0.5 to 10 mu g g(-1), and the limits of detection of the OPPs were in the range of 0.04-0.25 mu g g(-1). The method was satisfactorily applied to the analysis of real samples and is recommended for food control, research efforts when sample amounts are limited, and laboratories that have ordinary chromatographic instrumentation. (C) 2011 Elsevier B.V. All rights reserved.
Keywords: Matrix solid-phase dispersion, Solid-phase extraction, On-line coupling
ISI Document Delivery No.: 824ZU

1405. Valentine, G. W.; Mason, G. F.; Gomez, R.; Fasula, M.; Watzl, J.; Pittman, B.; Krystal, J. H., and Sanacora, G. The Antidepressant Effect of Ketamine Is Not Associated With Changes in Occipital Amino Acid Neurotransmitter Content as Measured by [(1)H]-Mrs.


Rec #: 76099
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: Psychopharmacology (Berl). 1992;106(2):285-7 (medline /1312732)
COMMENTS: Cites: Am J Psychiatry. 1997 Jun;154(6):805-11 (medline /9167508)
COMMENTS: Cites: Magn Reson Med. 1993 Dec;30(6):672-9 (medline /8139448)
COMMENTS: Cites: J Neurosci. 1997 Apr 1;17(7):2492-8 (medline /9065509)
COMMENTS: Cites: J Neurosci. 1997 Apr 15;17(8):2921-7 (medline /9092613)
COMMENTS: Cites: Biol Psychiatry. 2000 Feb 15;47(4):351-4 (medline /10686270)
COMMENTS: Cites: Behav Pharmacol. 1999 Feb;10(1):63-71 (medline /10780303)
COMMENTS: Cites: Eur J Neurosci. 2001 Feb;13(3):512-20 (medline /11168558)
COMMENTS: Cites: Magn Reson Med. 2001 Mar;45(3):517-20 (medline /11241712)
COMMENTS: Cites: Am J Psychiatry. 2002 Apr;159(4):663-5 (medline /11925309)
COMMENTS: Cites: Neurobiol Aging. 2003 Mar-Apr;24(2):273-84 (medline /12498961)
COMMENTS: Cites: Am J Psychiatry. 2003 Mar;160(3):577-9 (medline /12611844)
COMMENTS: Cites: Arch Gen Psychiatry. 2004 Jul;61(7):705-13 (medline /15237082)
COMMENTS: Cites: Biol Psychiatry. 2004 Sep 1;56(5):317-22 (medline /15336513)
COMMENTS: Cites: J Magn Reson. 2004 Oct;170(2):290-8 (medline /15388093)
COMMENTS: Cites: Am J Psychiatry. 2005 Feb;162(2):394-6 (medline /15677610)
COMMENTS: Cites: Arch Gen Psychiatry. 2006 Aug;63(8):856-64 (medline /16894061)
COMMENTS: Cites: Biol Psychiatry. 2008 Feb 15;63(4):349-52 (medline /17643398)
COMMENTS: Cites: Prog Neuropsychopharmacol Biol Psychiatry. 2008 Jan 1;32(1):140-4 (medline /17884272)
COMMENTS: Cites: Nat Rev Drug Discov. 2008 May;7(5):426-37 (medline /18425072)
COMMENTS: Cites: J Clin Psychopharmacol. 2008 Dec;28(6):631-7 (medline /19011431)
COMMENTS: Cites: Science. 2010 Aug 20;329(5994):959-64 (medline /20724638)
COMMENTS: Cites: Neurosci Lett. 2006 Jan 9;392(1-2):5-9 (medline /16183195)
COMMENTS: Cites: Magn Reson Med. 1994 Sep;32(3):294-302 (medline /7984061)
ABSTRACT: The NMDA receptor antagonist ketamine can induce a rapid improvement in depressive symptoms that often endures for days after a single intravenous dose. The pharmacodynamic basis for this effect is poorly understood. Using a proton magnetic resonance spectroscopy ([(1)H]-MRS) method that previously detected a normalization of amino acid neurotransmitter (AANt) content after chronic treatment with conventional antidepressant treatments, we examined whether the acute action of ketamine is associated with alterations in AANt content as well. Ten subjects with major depressive disorder (MDD) received saline, then ketamine in a fixed order, one week apart, under single-blind conditions. Each infusion was associated with three [(1)H] MRS scans (baseline, 3h and 48 h post-infusion) that measured glutamate, GABA and glutamine within the occipital cortex. Rating scales were administered before, during and after each infusion. The rapid (1h) and sustained (at least 7 days) antidepressant effect we observed after ketamine infusion was not associated with either baseline measures of, or changes in, occipital AANt content. Dissociative symptoms were not correlated with changes in depression scores. While our results indicate that changes in occipital AANt content are not a correlate of ketamine's antidepressant action, this may only apply to the regional and temporal windows of our MRS measurements.
MESH HEADINGS: Adult
MESH HEADINGS: Aged
MESH HEADINGS: Antidepressive Agents/*pharmacology/therapeutic use
MESH HEADINGS: Blood Pressure/drug effects
MESH HEADINGS: Depressive Disorder, Major/drug therapy/pathology
MESH HEADINGS: Dissociative Disorders/chemically induced
MESH HEADINGS: Female
MESH HEADINGS: Glutamic Acid/*metabolism
MESH HEADINGS: Heart Rate/drug effects
MESH HEADINGS: Humans
MESH HEADINGS: Ketamine/*pharmacology/therapeutic use
MESH HEADINGS: Magnetic Resonance Spectroscopy
MESH HEADINGS: Male
MESH HEADINGS: Middle Aged
MESH HEADINGS: Occipital Lobe/*drug effects/*metabolism
MESH HEADINGS: Protons/diagnostic use
MESH HEADINGS: Psychiatric Status Rating Scales
MESH HEADINGS: Psychometrics
MESH HEADINGS: Retrospective Studies
MESH HEADINGS: Single-Blind Method
MESH HEADINGS: Statistics as Topic
MESH HEADINGS: Time Factors
MESH HEADINGS: Young Adult
MESH HEADINGS: gamma-Aminobutyric Acid/*metabolism eng

1406. Valiyaveettil, Manojkumar; Alamneh, Yonas; Biggemann, Lionel; Soojhawon, Iswarduth; Doctor, Bhupendra P., and Nambiar, Madhusoodana P. Efficient hydrolysis of the chemical warfare nerve agent tabun by recombinant and purified human and rabbit serum paraoxonase 1. 2010 Dec 3-; 403, (1): 97-102.


Rec #: 2940
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Paraoxonase 1 (PON1) has been described as an efficient catalytic bioscavenger due to its ability to hydrolyze organophosphates (OPs) and chemical warfare nerve agents (CWNAs). It is the future most promising candidate as prophylactic medical countermeasure against highly toxic OPs and CWNAs. Most of the studies conducted so far have been focused on the hydrolyzing potential of PON1 against nerve agents, sarin, soman, and VX. Here, we investigated the hydrolysis of
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