Appendix 2-5: Rejected ecotox bibliography for Chlorpyrifos

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Keywords: Organophosphates
Keywords: Water Pollutants, Chemical -- analysis
Keywords: Risk Assessment
Keywords: Soil
Keywords: Ecosystem
Keywords: California
Keywords: 0
Keywords: Water Pollutants, Chemical -- adverse effects
Keywords: Pesticides
Keywords: Water Pollutants, Chemical
Keywords: Soil -- analysis
Keywords: Models, Chemical
Keywords: Organophosphates -- analysis
Keywords: Geographic Information Systems
Date completed - 2009-04-23
Date created - 2009-02-26
Date revised - 2012-12-20
Language of summary - English
Pages - 664-674
ProQuest ID - 66967015
Last updated - 2013-01-19
British nursing index edition - Journal of environmental quality, March 2009, 38(2):664-674
Corporate institution author - Luo, Yuzhou; Zhang, Minghua
DOI - MEDL-19244487; 19244487; 0047-2425 eng

828. Luo, Yuzhou ; Zhang, Minghua, and Luo, Yuzhou. Spatially Distributed Pesticide Exposure Assessment in the Central Valley, California, Usa. 2010 May; 158, (5): 1629-1637.

Rec #: 44139
Keywords: FATE
Notes: Chemical of Concern: CPY
Abstract: Abstract: Field runoff is an important transport mechanism by which pesticides move into the hydrologic environment of intensive agricultural regions such as California's Central Valley. This study presents a spatially explicit modeling approach to extend Pesticide Root Zone Model (PRZM), a field-scale pesticide transport model, into basin level. The approach was applied to simulate chlorpyrifos use in the Central Valley during 2003-2007. The average value of loading as percent of use (LAPU) is 0.031%. Results of this study provide strong evidence that surface runoff generation and pesticide application timing are the two influencing factors on the spatial and temporal variability of chlorpyrifos sources from agricultural fields. This is one of the first studies in coupling GIS and field-scale models and providing simulations for the dynamics of pesticides over an agriculturally dominated landscape. The demonstrated modeling approach may be useful for implementations of best management practice (BMP) and total maximum daily load (TMDL). Runoff generation and application timing are governing factors on spatiotemporal variability of pesticide sources.
Keywords: Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE)
Date revised - 2013-01-01
Language of summary - English
Pages - 1629-1637
ProQuest ID - 746150977
Last updated - 2013-01-07
British nursing index edition - Environmental Pollution [Environ. Pollut.]. Vol. 158, no. 5, pp. 1629-1637. May 2010.
Corporate institution author - Luo, Yuzhou; Zhang, Minghua
DOI - d8d6124a-cc60-4555-92e9csaobj201; 13028247; 0269-7491 English

829. Lurling, M. and Scheffer, M. Info-disruption: pollution and the transfer of chemical information between organisms. 2007; 22, (7): 374-379.

Rec #: 64569
Keywords: REVIEW
Notes: Chemical of Concern: CPY
Abstract: Abstract: Many organisms use subtle chemical cues not only to find partners and food, but also to sense the presence of natural enemies and to avoid predation. As we discuss here, an increasing number of studies now show that low, non-toxic concentrations of chemicals, ranging from heavy metals and pesticides to seemingly harmless substances such as surfactants, can disrupt the transfer of chemical information, inducing maladaptive responses in both the signaller and the receiver. Similar to endocrine disruptors, these 'info disruptors' form a new class of chemical threats, which could have far-reaching implications for ecosystem functioning and conservation management.
ISI Document Delivery No.: 189BF

830. Lusk, E. E. and Willis, J. D. The Development of Midge Problems in the Shasta Mosquito Abatement District. 1969; 37, 114(ABS).

Rec #: 1080
Keywords: NO TOX DATA
Notes: Chemical of Concern: CPY,EPRN,FNT,MP,PRN

831. Mű Zes, G.; Moln, R. B, and Sipos, F. Regulatory T Cells in Inflammatory Bowel Diseases and Colorectal Cancer.

Rec #: 49879
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: Scand J Immunol. 2011 Jul;74(1):47-51 (medline /21352252)
COMMENTS: Cites: J Immunol. 2011 Apr 1;186(7):4388-95 (medline /21357259)
COMMENTS: Cites: Int J Hematol. 2011 Mar;93(3):294-300 (medline /21374075)
COMMENTS: Cites: Science. 2011 Mar 25;331(6024):1565-70 (medline /21436444)
COMMENTS: Cites: J Immunol. 2011 Jun 1;186(11):6515-20 (medline /21515792)
COMMENTS: Cites: Science. 1990 Jan 19;247(4940):322-4 (medline /2296722)
COMMENTS: Cites: Dig Dis Sci. 1999 Apr;44(4):830-5 (medline /10219845)
COMMENTS: Cites: J Biol Chem. 2000 Jun 2;275(22):16979-85 (medline /10748032)
COMMENTS: Cites: J Exp Med. 2001 Jun 4;193(11):1303-10 (medline /11390437)
COMMENTS: Cites: Cell. 2002 Apr 5;109(1):113-24 (medline /11955451)
COMMENTS: Cites: Am J Physiol Gastrointest Liver Physiol. 2002 Jun;282(6):G1035-44 (medline /12016129)
COMMENTS: Cites: Int Arch Allergy Immunol. 2002 Dec;129(4):263-76 (medline /12483031)
COMMENTS: Cites: Science. 2003 Feb 14;299(5609):1057-61 (medline /12522256)
COMMENTS: Cites: Am J Pathol. 2003 Feb;162(2):691-702 (medline /12547727)
COMMENTS: Cites: Clin Cancer Res. 2003 Feb;9(2):606-12 (medline /12576425)
COMMENTS: Cites: Clin Exp Immunol. 2003 Oct;134(1):120-6 (medline /12974764)
COMMENTS: Cites: Cancer Res. 2003 Sep 15;63(18):6042-50 (medline /14522933)
COMMENTS: Cites: Gastroenterology. 2004 Jun;126(7):1759-70 (medline /15188171)
COMMENTS: Cites: Nat Med. 2004 Sep;10(9):942-9 (medline /15322536)
COMMENTS: Cites: Immunity. 2005 Mar;22(3):329-41 (medline /15780990)
COMMENTS: Cites: J Exp Med. 2005 Apr 4;201(7):1061-7 (medline /15809351)
COMMENTS: Cites: Gastroenterology. 2005 Jun;128(7):1868-78 (medline /15940622)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9253-7 (medline /15961541)
COMMENTS: Cites: Annu Rev Immunol. 2006;24:209-26 (medline /16551248)
COMMENTS: Cites: Nature. 2006 May 11;441(7090):231-4 (medline /16648837)
COMMENTS: Cites: Nature. 2006 May 11;441(7090):235-8 (medline /16648838)
COMMENTS: Cites: Inflamm Bowel Dis. 2006 Jun;12(6):447-56 (medline /16775488)
COMMENTS: Cites: Blood. 2006 Aug 1;108(3):804-11 (medline /16861339)
COMMENTS: Cites: Cancer Res. 2006 Aug 1;66(15):7395-400 (medline /16885333)
COMMENTS: Cites: J Exp Med. 2006 Oct 30;203(11):2485-94 (medline /17030948)
COMMENTS: Cites: Annu Rev Immunol. 2007;25:267-96 (medline /17134371)
COMMENTS: Cites: Cancer Immun. 2007;7:7 (medline /17388261)
COMMENTS: Cites: Lancet. 2007 May 12;369(9573):1627-40 (medline /17499605)
COMMENTS: Cites: J Exp Med. 2007 Jun 11;204(6):1405-16 (medline /17535971)
COMMENTS: Cites: Nat Immunol. 2007 Sep;8(9):967-74 (medline /17581537)
COMMENTS: Cites: J Exp Med. 2007 Aug 6;204(8):1849-61 (medline /17635957)
COMMENTS: Cites: Carcinogenesis. 2007 Dec;28(12):2614-23 (medline /17724375)
COMMENTS: Cites: Curr Opin Immunol. 2007 Dec;19(6):652-7 (medline /17766098)
COMMENTS: Cites: J Exp Med. 2007 Oct 1;204(10):2473-85 (medline /17893201)
COMMENTS: Cites: Clin Immunol. 2007 Dec;125(3):281-90 (medline /17897887)
COMMENTS: Cites: Nat Immunol. 2007 Dec;8(12):1380-9 (medline /17994022)
COMMENTS: Cites: Semin Immunol. 2007 Dec;19(6):362-71 (medline /18035554)
COMMENTS: Cites: Int J Cancer. 2008 Jun 1;122(11):2535-41 (medline /18246596)
COMMENTS: Cites: Nature. 2008 May 8;453(7192):236-40 (medline /18368049)
COMMENTS: Cites: Cancer Lett. 2008 Aug 28;267(2):271-85 (medline /18439751)
COMMENTS: Cites: Blood. 2008 Sep 15;112(6):2340-52 (medline /18617638)
COMMENTS: Cites: Cancer Cell. 2008 Sep 9;14(3):226-37 (medline /18772112)
COMMENTS: Cites: Immunology. 2009 Jun;127(2):196-205 (medline /18800986)
COMMENTS: Cites: Immunology. 2009 Jul;127(3):418-28 (medline /19016907)
COMMENTS: Cites: J Clin Oncol. 2009 Jan 10;27(2):186-92 (medline /19064967)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1027-32 (medline /19164562)
COMMENTS: Cites: Cancer Cell. 2009 Feb 3;15(2):79-80 (medline /19185839)
COMMENTS: Cites: Methods Enzymol. 2009;460:105-21 (medline /19446722)
COMMENTS: Cites: J Dig Dis. 2011 Aug;12(4):286-94 (medline /21791023)
COMMENTS: Cites: J Clin Immunol. 2011 Dec;31(6):1095-104 (medline /21915633)
COMMENTS: Cites: J Invest Dermatol. 2012 Mar;132(3 Pt 2):864-71 (medline /22158548)
COMMENTS: Cites: World J Gastrointest Pathophysiol. 2011 Dec 15;2(6):114-22 (medline /22180846)
COMMENTS: Cites: Cancer Res. 2012 Mar 1;72(5):1092-102 (medline /22282655)
COMMENTS: Cites: Gastroenterology. 2003 Mar;124(3):762-77 (medline /12612914)
COMMENTS: Cites: JAMA. 2001 Feb 7;285(5):643-7 (medline /11176874)
COMMENTS: Cites: Blood. 2009 Aug 6;114(6):1141-9 (medline /19470694)
COMMENTS: Cites: Clin Immunol. 2009 Oct;133(1):22-6 (medline /19559653)
COMMENTS: Cites: J Exp Med. 2009 Jul 6;206(7):1457-64 (medline /19564351)
COMMENTS: Cites: Gastroenterology. 2009 Oct;137(4):1270-9 (medline /19577568)
COMMENTS: Cites: Mediators Inflamm. 2009;2009:580450 (medline /19657406)
COMMENTS: Cites: Toxicol Pathol. 2010 Jan;38(1):76-87 (medline /20019355)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6430-5 (medline /20308560)
COMMENTS: Cites: Gastroenterology. 2011 Mar;140(3):957-65 (medline /21147109)
COMMENTS: Cites: World J Gastroenterol. 2011 Jan 21;17(3):343-8 (medline /21253393)
ABSTRACT: Regulatory T cells (T(regs)) are key elements in immunological self-tolerance. The number of T(regs) may alter in both peripheral blood and in colonic mucosa during pathological circumstances. The local cellular, microbiological and cytokine milieu affect immunophenotype and function of T(regs). Forkhead box P3+ T(regs) function shows altered properties in inflammatory bowel diseases (IBDs). This alteration of T(regs) function can furthermore be observed between Crohn's disease and ulcerative colitis, which may have both clinical and therapeutical consequences. Chronic mucosal inflammation may also influence T(regs) function, which together with the intestinal bacterial flora seem to have a supporting role in colitis-associated colorectal carcinogenesis. T(regs) have a crucial role in the immunoevasion of cancer cells in sporadic colorectal cancer. Furthermore, their number and phenotype correlate closely with the clinical outcome of the disease, even if their contribution to carcinogenesis has previously been controversial. Despite knowledge of the clinical relationship between IBD and colitis-associated colon cancer, and the growing number of immunological aspects encompassing sporadic colorectal carcinogenesis, the molecular and cellular links amongst T(regs), regulation of the inflammation, and cancer development are still not well understood. In this paper, we aimed to review the current data surrounding the role of T(regs) in the pathogenesis of IBD, colitis-associated colon cancer and sporadic colorectal cancer. eng

832. Ma, M; Zhang, B; Ge, Y-Z; Li, S-C, and Ma, M. Determination of the Activity of Acetylcholinesterase (Ache) in Pardosa Astrigera and the Inhibition Effects of Pesticides on Its Activity. 2011; 2, (1): 60-63.

Rec #: 43579
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: [Objective] The paper was to systemically study the characteristics of acetyl cholinesterase (AChE) in Pardosa astrigera, and confirm the occurrence and development of its pesticide resistance and the resistance level, thereby establishing a quick and accurate detection method for enzyme activity. [Method] The optimal conditions for assaying the activity of AChE in different parts of P. astrigera were determined by orthogonal experiment. The distribution conditions of acetyl cholinesterase (AChE) in different tissues of P. astrigera were further studied, and the sensitivities of the enzyme to four common pesticides were also determined. [Result] The optimal condition for assaying the activity of AChE in cephalothorax, abdomen and appendage of P. astrigera was as follows, enzyme concentrations: 12, 18 and 29 g/L; substrate concentrations: 0.6, 1.0 and 1.0 mmol/L; pH value, 7.0; reaction temperatures: 30, 35, 35 degree C; reaction time, 5 min. AChE was mainly distributed in the cephalothorax of P. astrigera. The specific activity of AChE in the extract solution with Triton X-100 was higher than that in the solution without Triton X-100. The median inhibitory concentrations (IC sub(50)) of methomyl, phoxim, betacypermethrin, chlorpyrifos against AChE in the cephalothorax of P. astrigera were 7.76 x 10 super(-5), 1.76 x 10 super(-4), 4.12 x 10 super(-4) and 4.94 x 10 super(-4) mol/L, respectively. [Conclusion] AChEs in P. astrigera were membrane-bounded. The inhibition of four pesticides against AChE in the cephalothorax of P. astrigera had good dose-effect, this indicated that AChE in the cephalothorax of P. astrigera could be used as the biochemical marker to monitor the contamination of organic phosphorus, carbamate and pyrethroid pesticides in the environment.
Keywords: Chlorpyrifos
Keywords: Plant diseases
Keywords: Biochemistry
Keywords: Pesticides
Keywords: Cephalothorax
Keywords: Enzymes
Keywords: Pests
Keywords: Cholinesterase
Keywords: Pollution Abstracts
Keywords: Pardosa astrigera
Keywords: Organic phosphorus
Date revised - 2012-11-01
Language of summary - English
Pages - 60-63
ProQuest ID - 1171875122
SubjectsTermNotLitGenreText - Chlorpyrifos; Plant diseases; Biochemistry; Pesticides; Cephalothorax; Enzymes; Pests; Cholinesterase; Organic phosphorus; Pardosa astrigera
Last updated - 2012-12-03
British nursing index edition - Plant Diseases and Pests. Vol. 2, no. 1, pp. 60-63. Feb 2011.
Corporate institution author - Zhang, B; Ge, Y-Z; Li, S-C
DOI - MD-0018594714; 16591868; 2152-3932 English

833. Macalady, D. L. and Wolfe, N. L. Effects of Sediment Sorption and Abiotic Hydrolyses. 1. Organophosphorothioate Esters. 1985; 33, 167-173.

Rec #: 1810
Keywords: FATE
Call Number: NO FATE (CPY,DZ)
Notes: Chemical of Concern: CPY,DZ

834. MacFarlane, E.; Benke, G.; Goddard, D., and Sim, M. Urban pest control operators in Australia. 2007; 64, (6): 422-427.

Rec #: 64579
Notes: Chemical of Concern: CPY
ISI Document Delivery No.: 169LS

835. Macomber, L.; Rensing, C., and Imlay, J. A. Intracellular Copper Does Not Catalyze the Formation of Oxidative Dna Damage in Escherichia Coli.

Rec #: 51459
Keywords: BACTERIA
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: Nat Genet. 1993 Dec;5(4):327-37 (medline /8298639)
COMMENTS: Cites: Nat Genet. 1993 Dec;5(4):344-50 (medline /8298641)
COMMENTS: Cites: Free Radic Biol Med. 1994 Jan;16(1):29-33 (medline /8299992)
COMMENTS: Cites: Carcinogenesis. 1993 Jul;14(7):1303-11 (medline /8392444)
COMMENTS: Cites: Mol Microbiol. 1999 Apr;32(1):179-91 (medline /10216871)
COMMENTS: Cites: J Bacteriol. 1999 Aug;181(15):4639-43 (medline /10419964)
COMMENTS: Cites: J Bacteriol. 1999 Oct;181(20):6223-9 (medline /10515908)
COMMENTS: Cites: J Bacteriol. 1999 Nov;181(21):6772-8 (medline /10542180)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):652-6 (medline /10639134)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6640-5 (medline /10829079)
COMMENTS: Cites: J Biol Chem. 2000 Oct 6;275(40):31024-9 (medline /10915804)
COMMENTS: Cites: J Bacteriol. 2000 Oct;182(20):5864-71 (medline /11004187)
COMMENTS: Cites: J Bacteriol. 2001 Mar;183(6):2145-7 (medline /11222619)
COMMENTS: Cites: J Biol Chem. 2001 Aug 17;276(33):30670-7 (medline /11399769)
COMMENTS: Cites: J Bacteriol. 2001 Aug;183(15):4562-70 (medline /11443091)
COMMENTS: Cites: J Bacteriol. 2001 Aug;183(15):4571-9 (medline /11443092)
COMMENTS: Cites: J Bacteriol. 2001 Aug;183(16):4866-75 (medline /11466290)
COMMENTS: Cites: Biochem Biophys Res Commun. 2001 Sep 7;286(5):902-8 (medline /11527384)
COMMENTS: Cites: J Mol Biol. 2001 Oct 5;312(5):1089-101 (medline /11580252)
COMMENTS: Cites: J Bacteriol. 2001 Dec;183(24):7173-81 (medline /11717276)
COMMENTS: Cites: J Bacteriol. 2001 Dec;183(24):7182-9 (medline /11717277)
COMMENTS: Cites: Methods Enzymol. 2002;349:3-9 (medline /11912920)
COMMENTS: Cites: J Biol Chem. 2002 Aug 2;277(31):27689-96 (medline /12016214)
COMMENTS: Cites: J Biol Chem. 2002 Sep 13;277(37):34055-66 (medline /12080063)
COMMENTS: Cites: Mol Microbiol. 2002 Aug;45(4):997-1005 (medline /12180919)
COMMENTS: Cites: J Bacteriol. 2003 Mar;185(6):1942-50 (medline /12618458)
COMMENTS: Cites: J Bacteriol. 2003 Jul;185(13):3804-12 (medline /12813074)
COMMENTS: Cites: Mol Microbiol. 2003 Jul;49(1):11-22 (medline /12823807)
COMMENTS: Cites: Genes Dev. 1992 Dec;6(12B):2646-54 (medline /1340475)
COMMENTS: Cites: J Bacteriol. 2003 Dec;185(23):6815-25 (medline /14617646)
COMMENTS: Cites: Toxicology. 2004 Mar 1;196(1-2):57-64 (medline /15036756)
COMMENTS: Cites: Ann Neurol. 2004 May;55(5):645-53 (medline /15122704)
COMMENTS: Cites: Comp Biochem Physiol C Toxicol Pharmacol. 2004 Apr;137(4):335-42 (medline /15228951)
COMMENTS: Cites: J Biol Chem. 2004 Oct 22;279(43):44590-9 (medline /15308657)
COMMENTS: Cites: Lancet. 1996 Mar 30;347(9005):877-80 (medline /8622397)
COMMENTS: Cites: Mol Gen Genet. 1996 May 23;251(2):139-45 (medline /8668123)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1996 Nov 26;93(24):13635-40 (medline /8942986)
COMMENTS: Cites: Am J Hum Genet. 1997 Aug;61(2):317-28 (medline /9311736)
COMMENTS: Cites: Science. 2004 Nov 5;306(5698):1025-8 (medline /15459345)
COMMENTS: Cites: Food Chem Toxicol. 2004 Dec;42(12):1931-6 (medline /15500930)
COMMENTS: Cites: J Bacteriol. 2004 Nov;186(22):7815-7 (medline /15516598)
COMMENTS: Cites: Biochem Biophys Res Commun. 2005 Feb 11;327(2):454-9 (medline /15629136)
COMMENTS: Cites: J Biol Inorg Chem. 2005 May;10(3):221-30 (medline /15770503)
COMMENTS: Cites: Mutat Res. 2005 May 2;583(1):75-84 (medline /15866468)
COMMENTS: Cites: Toxicol Appl Pharmacol. 2005 Nov 15;209(1):62-73 (medline /15882883)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9317-22 (medline /15967999)
COMMENTS: Cites: Biochemistry. 2005 Aug 9;44(31):10533-40 (medline /16060662)
COMMENTS: Cites: J Biol Chem. 2005 Oct 7;280(40):33785-91 (medline /16087673)
COMMENTS: Cites: Mutat Res. 2006 Jun 16;605(1-2):78-86 (medline /16697250)
COMMENTS: Cites: J Bacteriol. 1990 Aug;172(8):4197-205 (medline /1695893)
COMMENTS: Cites: Biochemistry. 2006 Sep 19;45(37):11096-102 (medline /16964970)
COMMENTS: Cites: J Biol Chem. 2007 Jan 12;282(2):929-37 (medline /17102132)
COMMENTS: Cites: Chem Biol Interact. 1976 Aug;14(3-4):347-56 (medline /182394)
COMMENTS: Cites: J Biol Chem. 1989 Apr 5;264(10):5598-605 (medline /2564391)
COMMENTS: Cites: Science. 1988 Apr 29;240(4852):640-2 (medline /2834821)
COMMENTS: Cites: Cell. 1985 Jul;41(3):753-62 (medline /2988786)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1986 Nov;83(21):8268-72 (medline /3022287)
COMMENTS: Cites: J Bacteriol. 1986 May;166(2):519-27 (medline /3516975)
COMMENTS: Cites: J Mol Biol. 1986 Sep 5;191(1):39-58 (medline /3540312)
COMMENTS: Cites: J Bacteriol. 1984 Feb;157(2):622-6 (medline /6319370)
COMMENTS: Cites: Methods Enzymol. 1984;105:3-22 (medline /6328186)
COMMENTS: Cites: Biochem J. 1984 Feb 15;218(1):273-5 (medline /6712613)
COMMENTS: Cites: Nat Genet. 1995 Feb;9(2):210-7 (medline /7626145)
COMMENTS: Cites: J Bacteriol. 1995 May;177(9):2305-14 (medline /7730258)
COMMENTS: Cites: Gene. 1995 May 26;158(1):9-14 (medline /7789817)
COMMENTS: Cites: Arch Biochem Biophys. 1995 Jan 10;316(1):515-22 (medline /7840659)
COMMENTS: Cites: Mol Microbiol. 1994 Jul;13(2):265-72 (medline /7984106)
COMMENTS: Cites: J Biol Chem. 1993 Oct 25;268(30):22369-76 (medline /8226748)
ABSTRACT: Because copper catalyzes the conversion of H(2)O(2) to hydroxyl radicals in vitro, it has been proposed that oxidative DNA damage may be an important component of copper toxicity. Elimination of the copper export genes, copA, cueO, and cusCFBA, rendered Escherichia coli sensitive to growth inhibition by copper and provided forcing circumstances in which this hypothesis could be tested. When the cells were grown in medium supplemented with copper, the intracellular copper content increased 20-fold. However, the copper-loaded mutants were actually less sensitive to killing by H(2)O(2) than cells grown without copper supplementation. The kinetics of cell death showed that excessive intracellular copper eliminated iron-mediated oxidative killing without contributing a copper-mediated component. Measurements of mutagenesis and quantitative PCR analysis confirmed that copper decreased the rate at which H(2)O(2) damaged DNA. Electron paramagnetic resonance (EPR) spin trapping showed that the copper-dependent H(2)O(2) resistance was not caused by inhibition of the Fenton reaction, for copper-supplemented cells exhibited substantial hydroxyl radical formation. However, copper EPR spectroscopy suggested that the majority of H(2)O(2)-oxidizable copper is located in the periplasm; therefore, most of the copper-mediated hydroxyl radical formation occurs in this compartment and away from the DNA. Indeed, while E. coli responds to H(2)O(2) stress by inducing iron sequestration proteins, H(2)O(2)-stressed cells do not induce proteins that control copper levels. These observations do not explain how copper suppresses iron-mediated damage. However, it is clear that copper does not catalyze significant oxidative DNA damage in vivo; therefore, copper toxicity must occur by a different mechanism.
MESH HEADINGS: Copper/analysis/*toxicity
MESH HEADINGS: Escherichia coli/growth &
MESH HEADINGS: development/*metabolism
MESH HEADINGS: Hydrogen Peroxide/toxicity
MESH HEADINGS: Hydroxyl Radical/metabolism
MESH HEADINGS: Iron/metabolism
MESH HEADINGS: Oxidation-Reduction
MESH HEADINGS: Periplasm/chemistry eng

836. Mage, D. T. Microg/Kg-Day or Microg/Day? A Commentary on Georgopoulos Et Al., Jesee 2008.

Rec #: 79369
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Comment on: J Expo Sci Environ Epidemiol. 2009 Feb;19(2):149-71 (medline /18368010)
MESH HEADINGS: Biological Markers/analysis/metabolism
MESH HEADINGS: Chlorpyrifos/administration &
MESH HEADINGS: dosage/metabolism/*toxicity
MESH HEADINGS: Dose-Response Relationship, Drug
MESH HEADINGS: Environmental Exposure/adverse effects/*analysis
MESH HEADINGS: Insecticides/administration &
MESH HEADINGS: dosage/metabolism/*toxicity
MESH HEADINGS: Public Health
MESH HEADINGS: Risk Assessment
MESH HEADINGS: Time Factors eng

837. Mage, D. T.; Allen, R. H., and Kodali, A. Creatinine corrections for estimating children's and adult's pesticide intake doses in equilibrium with urinary pesticide and creatinine concentrations. 2008; 18, (4): 360-368.

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