Appendix 2-5: Rejected ecotox bibliography for Chlorpyrifos



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OP-labeled lysine residues were found in seven proteins that had been treated with either chlorpyrifos oxon (CPO) or diisopropylfluorophosphate (DFP): human serum albumin (K212, K414, K199, and K351), human keratin 1 (K211 and K355), human keratin 10 (K163), bovine tubulin alpha (K60, K336, K163, K394, and K401), bovine tubulin beta (K58), bovine actin (K113, K291, K326, K315, and K328), and mouse transferrin (K296 and K626). These results suggest that OP binding to lysine is a general phenomenon. Characteristic fragments specific for CPO-labeled lysine appeared at 237.1, 220.0, 192.0, 163.9, 128.9, and 83.9 amu. Characteristic fragments specific for DFP-labeled lysine appeared at 164.0, 181.2, and 83.8 amu. This new OP-binding motif to lysine suggests new directions to search for mechanisms of long-term effects of OP exposure and in the search for biomarkers of OP exposure. Mass spectrometry/ Organophosphate esters/ Chlorpyrifos oxon/ Diisopropylfluorophosphate/ Serum albumin/ Keratin/ Tubulin/ Actin/ Transferrin

500. Grigoryan, Hasmik; Lockridge, Oksana, and Grigoryan, Hasmik. Nanoimages Show Disruption of Tubulin Polymerization by Chlorpyrifos Oxon: Implications for Neurotoxicity. 2009 Oct 15; 240, (2): 143-148.


Rec #: 40949
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: Organophosphorus agents cause cognitive deficits and depression in some people. We hypothesize that the mechanism by which organophosphorus agents cause these disorders is by modification of proteins in the brain. One such protein could be tubulin. Tubulin polymerizes to make the microtubules that transport cell components to nerve axons. The goal of the present work was to measure the effect of the organophosphorus agent chlorpyrifos oxon on tubulin polymerization. An additional goal was to identify the amino acids covalently modified by chlorpyrifos oxon in microtubule polymers and to compare them to the amino acids modified in unpolymerized tubulin dimers. Purified bovine tubulin (0.1AmM) was treated with 0.005a"0.1AmM chlorpyrifos oxon for 30Amin at room temperature and then polymerized by addition of 1AmM GTP to generate microtubules. Microtubules were visualized by atomic force microscopy. Chlorpyrifos oxon-modified residues were identified by tandem ion trap electrospray ionization and matrix-assisted laser desorption/ionization mass spectrometry of tryptic peptides. Nanoimaging showed that low concentrations (0.005 and 0.01AmM) of chlorpyrifos oxon yielded short, thin microtubules. A concentration of 0.025AmM stimulated polymerization, while high concentrations (0.05 and 0.1AmM) caused aggregation. Of the 17 tyrosines covalently modified by chlorpyrifos oxon in unpolymerized tubulin dimers, only 2 tyrosines were labeled in polymerized microtubules. The two labeled tyrosines in polymerized tubulin were Tyr 103 in EDAANNYaR of alpha tubulin, and Tyr 281 in GSQQYaR of beta tubulin. In conclusion, chlorpyrifos oxon binding to tubulin disrupts tubulin polymerization. These results may lead to an understanding of the neurotoxicity of organophosphorus agents.
Keywords: X 24390:Radioactive Materials
Keywords: CSA Neurosciences Abstracts; Toxicology Abstracts
Keywords: Temperature effects
Keywords: Microtubules
Keywords: Pharmacy And Pharmacology
Keywords: Amino acids
Keywords: Polymerization
Keywords: Depression
Keywords: N3 11028:Neuropharmacology & toxicology
Keywords: atomic force microscopy
Keywords: Brain
Keywords: GTP
Keywords: Tyrosine
Keywords: Mass spectroscopy
Keywords: Nerves
Keywords: Chlorpyrifos
Keywords: Cognitive ability
Keywords: Neurotoxicity
Keywords: Tryptic peptides
Keywords: Axons
Keywords: Lasers
Keywords: Tubulin
Keywords: Ionization
Date revised - 2010-02-01
Language of summary - English
Pages - 143-148
ProQuest ID - 810776830
SubjectsTermNotLitGenreText - Temperature effects; Microtubules; Depression; Polymerization; Amino acids; Brain; atomic force microscopy; Tyrosine; GTP; Mass spectroscopy; Nerves; Chlorpyrifos; Cognitive ability; Neurotoxicity; Tryptic peptides; Axons; Lasers; Tubulin; Ionization
Last updated - 2011-11-02
Corporate institution author - Grigoryan, Hasmik; Lockridge, Oksana
DOI - OB-6e6ce6c9-07fa-4559-a383csamfg201; 13008588; 0041-008X English

501. Grigoryan, Hasmik; Schopfer, Lawrence M; Peeples, Eric S; Duysen, Ellen G; Grigoryan, Marine; Thompson, Charles M; Lockridge, Oksana, and Grigoryan, Hasmik. Mass Spectrometry Identifies Multiple Organophosphorylated Sites on Tubulin. 2009 Oct 15; 240, (2): 149-158.


Rec #: 40959
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: Acute toxicity of organophosphorus poisons (OP) is explained by inhibition of acetylcholinesterase in nerve synapses. Low-dose effects are hypothesized to result from modification of other proteins, whose identity is not yet established. The goal of the present work was to obtain information that would make it possible to identify tubulin as a target of OP exposure. Tubulin was selected for study because live mice injected with a nontoxic dose of a biotinylated organophosphorus agent appeared to have OP-labeled tubulin in brain as determined by binding to avidin beads and mass spectrometry. The experiments with live mice were not conclusive because binding to avidin beads could be nonspecific. To be convincing, it is necessary to find and characterize the OP-labeled tubulin peptide. The search for OP-labeled tubulin peptides was begun by identifying residues capable of making a covalent bond with OP. Pure bovine tubulin (0.012AmM) was treated with 0.01a"0.5AmM chlorpyrifos oxon for 24Ah at 37AA degree C in pH 8.3 buffer. The identity of labeled amino acids and percent labeling was determined by mass spectrometry. Chlorpyrifos oxon bound covalently to tyrosines 83, 103, 108, 161, 224, 262, 272, 357, and 399 in bovine alpha tubulin, and to tyrosines 50, 51, 59, 106, 159, 281, 310, and 340 in bovine beta tubulin. The most reactive were tyrosine 83 in alpha and tyrosine 281 in beta tubulin. In the presence of 1AmM GTP, percent labeling increased 2-fold. Based on the crystal structure of the tubulin heterodimer (PDB 1jff) tyrosines 83 and 281 are well exposed to solvent. In conclusion seventeen tyrosines in tubulin have the potential to covalently bind chlorpyrifos oxon. These results will be useful when searching for OP-labeled tubulin in live animals.
Keywords: Synapses
Keywords: Pharmacy And Pharmacology
Keywords: Amino acids
Keywords: Acetylcholinesterase
Keywords: Solvents
Keywords: Brain
Keywords: Tyrosine
Keywords: GTP
Keywords: Acute toxicity
Keywords: Mass spectroscopy
Keywords: Chlorpyrifos
Keywords: Nerves
Keywords: Avidin
Keywords: Crystal structure
Keywords: Tubulin
Keywords: X 24330:Agrochemicals
Keywords: pH effects
Keywords: Toxicology Abstracts
Date revised - 2010-02-01
Language of summary - English
Pages - 149-158
ProQuest ID - 810697154
SubjectsTermNotLitGenreText - Synapses; Amino acids; Acetylcholinesterase; Brain; Solvents; GTP; Tyrosine; Acute toxicity; Mass spectroscopy; Nerves; Chlorpyrifos; Avidin; Crystal structure; Tubulin; pH effects
Last updated - 2011-11-02
Corporate institution author - Grigoryan, Hasmik; Schopfer, Lawrence M; Peeples, Eric S; Duysen, Ellen G; Grigoryan, Marine; Thompson, Charles M; Lockridge, Oksana
DOI - OB-9a1d2a5d-dbcc-42e8-8be9csamfg201; 13008586; 0041-008X English

502. Guducu, H. E.; Inam, R., and Aboul-Enein, H. Y. DETERMINATION OF ORGANOPHOSPHORUS AND TRIAZOLE PESTICIDES BY GAS CHROMATOGRAPHY AND APPLICATION TO VEGETABLE AND COMMERCIAL SAMPLES. 2011; 34, (19): 2473-2483.


Rec #: 60909
Keywords: CHEM METHODS
Notes: Chemical of Concern: CPY
Abstract: Abstract: A multiresidue method using gas chromatography with electron-capture detection (ECD), nitrogen-phosphorus detection (NPD), or flame ionization detection (FID) has been developed for the determination of triazole residues such as triadimefon, penconazole, hexaconazole, diniconazole, and organophosphorus residues such as chlorpyrifos-methyl. The method has been successfully applied to the analysis of tomatoes and eggplant samples. The recoveries obtained from NPD detector for tomatoes and eggplants were in the range 62.0-109% and 66.0-104% with the relative standard deviation varied from 5.0 to 13.1% and 3.2 to 18.0%, respectively. The method was validated and applied for the determination of triazole and organophosphorus pesticides in agrochemical formulations within the recoveries of 96.3-107.2%.
Keywords: agrochemical formulations analysis, food analysis, gas chromatography,
ISI Document Delivery No.: 880AI

503. Guiã±Azãº, Natalia; Rena, Viviana; Genti-Raimondi, Susana; Rivero, Virginia, and Magnarelli, Gladis. Effects of the Organophosphate Insecticides Phosmet and Chlorpyrifos on Trophoblast Jeg-3 Cell Death, Proliferation and Inflammatory Molecule Production. 2012 Apr; 26, (3): 406-413.


Rec #: 38929
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: Epidemiological data have associated environmental organophosphate insecticide (OP) exposure during pregnancy with fetal growth deficits. To better understand OP injury that may adversely affect pregnancy, we used the JEG-3 choriocarcinoma cell line, which provide a recognized in vitro model to study placental function. The effects of the OP phosmet (Pm) and chlorpyrifos (Cp) on JEG-3 cells viability, proliferation, cell cycle and inflammatory molecule production were evaluated. Both insecticides affected cellular viability in a concentration- and time-dependent manner, inducing apoptosis and decreasing [(3)H]-thymidine incorporation. However, only Pm reduced DNA synthesis independently of cellular death and decreased the cell percentage at the S-phase. Unlike apoptosis, TNFα production varied with the concentration tested, suggesting that other TNFα independent mechanisms might trigger cell death. No induction of the inflammatory molecule nitric oxide was detected. The mRNA levels of pro-inflammatory IL-6, IL-17 and the anti-inflammatory IL-13 cytokines were differentially modulated. These findings show that Pm and Cp generate a specific toxicity signature, altering cell viability and inducing an inflammatory cytokine profile, suggesting that trophoblasts may represent a possible target for OP adverse effects. Copyright © 2012 Elsevier Ltd. All rights reserved.
Keywords: Phosmet
Keywords: 2921-88-2
Keywords: Trophoblasts -- pathology
Keywords: Insecticides -- administration & dosage
Keywords: Humans
Keywords: Trophoblasts -- drug effects
Keywords: Nitric Oxide -- metabolism
Keywords: Choriocarcinoma -- pathology
Keywords: Insecticides
Keywords: Cell Survival -- drug effects
Keywords: 732-11-6
Keywords: Apoptosis -- drug effects
Keywords: Inflammation Mediators
Keywords: Cytokines
Keywords: Time Factors
Keywords: Insecticides -- toxicity
Keywords: Cell Proliferation -- drug effects
Keywords: Chlorpyrifos -- administration & dosage
Keywords: Dose-Response Relationship, Drug
Keywords: Cell Line, Tumor
Keywords: Cytokines -- metabolism
Keywords: Cell Death -- drug effects
Keywords: 10102-43-9
Keywords: Pregnancy
Keywords: Inflammation Mediators -- metabolism
Keywords: Chlorpyrifos
Keywords: Nitric Oxide
Keywords: RNA, Messenger
Keywords: 0
Keywords: Chlorpyrifos -- toxicity
Keywords: Phosmet -- toxicity
Keywords: RNA, Messenger -- metabolism
Keywords: Phosmet -- administration & dosage
Keywords: Female
Date completed - 2012-06-26
Date created - 2012-03-05
Date revised - 2012-12-20
Language of summary - English
Pages - 406-413
ProQuest ID - 926504803
Last updated - 2013-01-19
British nursing index edition - Toxicology in vitro : an international journal published in association with BIBRA, April 2012, 26(3):406-413
Corporate institution author - Guiñazú, Natalia; Rena, Viviana; Genti-Raimondi, Susana; Rivero, Virginia; Magnarelli, Gladis
DOI - MEDL-22265773; 22265773; 1879-3177 eng

504. Gunier, Robert B; Ward, Mary H; Airola, Matthew; Bell, Erin M; Colt, Joanne; Nishioka, Marcia; Buffler, Patricia a; Reynolds, Peggy; Rull, Rudolph P; Hertz, Andrew; Metayer, Catherine; Nuckols, John R, and Gunier, Robert B. Determinants of Agricultural Pesticide Concentrations in Carpet Dust. 2011 Feb 17; 119, (7): 970-976.


Rec #: 43549
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: Background: Residential proximity to agricultural pesticide applications has been used as a surrogate for exposure in epidemiologic studies, although little is known about the relationship with levels of pesticides in homes. Objective: We identified determinants of concentrations of agricultural pesticides in dust. Methods: We collected samples of carpet dust and mapped crops within 1,250 m of 89 residences in California. We measured concentrations of seven pesticides used extensively in agriculture (carbaryl, chlorpyrifos, chlorthal-dimethyl, diazinon, iprodione, phosmet, and simazine). We estimated use of agricultural pesticides near residences from a statewide database alone and by linking the database with crop maps. We calculated the density of pesticide use within 500 and 1,250 m of residences for 180, 365, and 730 days before collection of dust and evaluated relationships between agricultural pesticide use estimates and pesticide concentrations in carpet dust. Results: For five of the seven pesticides evaluated, residences with use of agricultural pesticides within 1,250 m during the previous 365 days had significantly higher concentrations of pesticides than did residences with no nearby use. The highest correlation with concentrations of pesticides was generally for use reported within 1,250 m of the residence and 730 days before sample collection. Regression models that also accounted for occupational and home use of pesticides explained only a modest amount of the variability in pesticide concentrations (4-28%). Conclusions: Agricultural pesticide use near residences was a significant determinant of concentrations of pesticides in carpet dust for five of seven pesticides evaluated.
Keywords: agriculture
Keywords: Carbaryl
Keywords: Simazine
Keywords: Herbicides
Keywords: Dust
Keywords: Crops
Keywords: Environmental Studies
Keywords: ENA 02:Toxicology & Environmental Safety
Keywords: Chlorpyrifos
Keywords: Pesticides
Keywords: Environment Abstracts
Keywords: USA, California
Keywords: Diazinon
Date revised - 2012-03-01
Language of summary - English
Location - USA, California
Pages - 970-976
ProQuest ID - 919376237
SubjectsTermNotLitGenreText - Chlorpyrifos; Pesticides; agriculture; Carbaryl; Herbicides; Simazine; Diazinon; Crops; Dust; USA, California
Last updated - 2012-08-08
Corporate institution author - Gunier, Robert B; Ward, Mary H; Airola, Matthew; Bell, Erin M; Colt, Joanne; Nishioka, Marcia; Buffler, Patricia A; Reynolds, Peggy; Rull, Rudolph P; Hertz, Andrew; Metayer, Catherine; Nuckols, John R
DOI - OB-fc767b71-088c-4284-8114csamfg201; 16210168; 0091-6765; 1552-9924 English

505. Guo, Xishan ; Zhang, Xueyin; Cai, Qiang; Shen, Tao, and Zhu, Songming. Developing a novel sensitive visual screening card for rapid detection of pesticide residues in food. 2013 Mar; 30, (1): 15-23.


Rec #: 5060
Keywords: FOOD
Notes: Chemical of Concern: CPY
Abstract: A novel sensitive visual screening card for rapid detection of pesticide residues was developed based on the blue-green color intensity changes, which were generated as a result of indoxyl acetate hydrolysis catalyzed by acetylcholinesterase (AChE) and the inhibition of AChE activity by pesticides. The procedure for preparing the test card was optimized. The AChE was immobilized onto the Hybond N+ nylon membrane using physical adsorption method. The immobilization temperature was set at 4-á-_C and the immobilization time was set to 30-ámin. The immobilized enzyme was freeze dried under vacuum conditions for 2-ámin. The indoxyl acetate was dissolved in methanol and diluted to 10-ámM by phosphate buffer solution (pH7.5). The inhibition time and the color development time were set to 15-ámin and 10-ámin respectively. The final experimental results on determining various pesticides showed that the limit of detection (LOD) of this assay system was 1-á++g/mL for omethoate, 0.1-á++g/mL for dichlorvos, 2-á++g/mL for methamidophos, 0.05-á++g/mL for chlorpyrifos, 1.5-á++g/mL for carbaryl, and 0.8-á++g/mL for pirimicarb. Detection results of pesticide residues in real food samples of fruit juices and vegetable showed this visual screening card had high sensitivity, good reproducibility and stable-storage property, suggesting its great potential for practical application in rapid determination of pesticide residues. Pesticide residues/ Acetylcholinesterase/ Indoxyl acetate hydrolysis/ Rapid determination

506. Gupta, S. and Gajbhiye, V. T. Persistence of acetamiprid in soil. 2007; 78, (5): 349-352.


Rec #: 61019
Keywords: FATE
Notes: Chemical of Concern: CPY
Abstract: Keywords: ALLUVIAL SOIL, CHLORPYRIFOS, MOISTURE
ISI Document Delivery No.: 195JZ

507. Gupta, S.; Gajbhiye, V. T.; Sharma, R. K., and Gupta, R. K. Dissipation of Cypermethrin, Chlorpyriphos, and Profenofos in Tomato Fruits and Soil Following Application of Pre-Mix Formulations. Springer Science & Business Media//: SOIL; 2011; 174, (1-4): 337-345.


Rec #: 2650
Keywords: MIXTURE
Call Number: NO MIXTURE (CPY,CYP,IMC,PFF)
Notes: Chemical of Concern: CPY,CYP,PFF

508. Gurevich, I.; Zhang, C.; Encarnacao, P. C.; Struzynski, C. P.; Livings, S. E., and Aneskievich, B. J. PparΓ and Nf-ΚB Regulate the Gene Promoter Activity of Their Shared Repressor, Tnip1.


Rec #: 73379
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: J Lipid Res. 2003 Apr;44(4):686-95 (medline /12562861)
COMMENTS: Cites: FEBS Lett. 2003 Feb 11;536(1-3):135-40 (medline /12586352)
COMMENTS: Cites: Annu Rev Biochem. 2003;72:449-79 (medline /12651739)
COMMENTS: Cites: Gene. 2003 Aug 14;313:43-57 (medline /12957376)
COMMENTS: Cites: FEBS Lett. 2003 Sep 11;551(1-3):8-12 (medline /12965196)
COMMENTS: Cites: J Biol Chem. 2003 Nov 7;278(45):43889-92 (medline /14506269)
COMMENTS: Cites: J Acquir Immune Defic Syndr. 2003 Oct 1;34(2):127-33 (medline /14526201)
COMMENTS: Cites: Mol Endocrinol. 2005 Mar;19(3):595-606 (medline /15563547)
COMMENTS: Cites: Mol Pharmacol. 2005 Apr;67(4):1257-67 (medline /15635043)
COMMENTS: Cites: J Biol Chem. 2005 May 6;280(18):17938-44 (medline /15722346)
COMMENTS: Cites: J Biol Chem. 2005 Apr 29;280(17):17435-48 (medline /15722553)
COMMENTS: Cites: Biochim Biophys Acta. 2005 Apr 5;1728(1-2):95-104 (medline /15777674)
COMMENTS: Cites: Photochem Photobiol. 2008 Mar-Apr;84(2):515-21 (medline /18266815)
COMMENTS: Cites: J Biol Chem. 2006 Jul 7;281(27):18482-8 (medline /16684768)
COMMENTS: Cites: Mol Cell Biol. 2006 Aug;26(15):5698-714 (medline /16847324)
COMMENTS: Cites: Genes Dev. 2006 Sep 15;20(18):2513-26 (medline /16980581)
COMMENTS: Cites: FEBS Lett. 2008 Jan 9;582(1):39-45 (medline /18023280)
COMMENTS: Cites: Oncogene. 2008 Jun 12;27(26):3739-45 (medline /18212736)
COMMENTS: Cites: Carcinogenesis. 2008 Oct;29(10):1938-43 (medline /18676680)
COMMENTS: Cites: Genes Dev. 2008 Aug 1;22(15):2093-101 (medline /18676814)
COMMENTS: Cites: Nature. 2009 Feb 12;457(7231):906-9 (medline /19060883)
COMMENTS: Cites: Nat Genet. 2009 Feb;41(2):199-204 (medline /19169254)
COMMENTS: Cites: J Cell Physiol. 2009 Aug;220(2):427-39 (medline /19388012)
COMMENTS: Cites: Hum Gene Ther. 2009 Sep;20(9):1005-12 (medline /19499975)
COMMENTS: Cites: Biochem Biophys Res Commun. 2009 Nov 20;389(3):409-14 (medline /19732752)
COMMENTS: Cites: Biochemistry. 1993 Jun 1;32(21):5598-604 (medline /7684926)
COMMENTS: Cites: J Virol. 1994 Dec;68(12):8035-44 (medline /7966593)
COMMENTS: Cites: Nature. 1998 Sep 10;395(6698):137-43 (medline /9744270)
COMMENTS: Cites: FEBS Lett. 1999 Jan 8;442(1):83-8 (medline /9923610)
COMMENTS: Cites: J Cell Biol. 1999 Jun 28;145(7):1471-82 (medline /10385526)
COMMENTS: Cites: J Biol Chem. 1999 Dec 10;274(50):35881-8 (medline /10585473)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4844-9 (medline /10781090)
COMMENTS: Cites: Mol Cell Biol. 2000 Jul;20(13):4699-707 (medline /10848596)
COMMENTS: Cites: J Biol Chem. 2000 Oct 20;275(42):32681-7 (medline /10934192)
COMMENTS: Cites: Biochem Pharmacol. 2000 Oct 15;60(8):1143-51 (medline /11007952)
COMMENTS: Cites: J Virol. 2000 Dec;74(24):11811-24 (medline /11090181)
COMMENTS: Cites: Kidney Int. 2001 Jun;59(6):2174-81 (medline /11380819)
COMMENTS: Cites: J Biol Chem. 2002 May 10;277(19):16913-9 (medline /11847231)
COMMENTS: Cites: J Cell Biochem. 2002;85(1):72-82 (medline /11891851)
COMMENTS: Cites: Cell. 2002 Apr 5;109(1):125-35 (medline /11955452)
COMMENTS: Cites: J Biol Chem. 2002 Jul 26;277(30):26821-30 (medline /12015306)
COMMENTS: Cites: Int J Mol Med. 2006 Nov;18(5):917-23 (medline /17016622)
COMMENTS: Cites: J Steroid Biochem Mol Biol. 2006 Dec;102(1-5):51-9 (medline /17056252)
COMMENTS: Cites: Oncogene. 2006 Oct 30;25(51):6868-86 (medline /17072333)
COMMENTS: Cites: Biochem Biophys Res Commun. 2007 Apr 6;355(2):494-500 (medline /17306764)
COMMENTS: Cites: J Biol Chem. 2007 Apr 13;282(15):11530-9 (medline /17307735)
COMMENTS: Cites: Endocr Rev. 2007 Aug;28(5):575-87 (medline /17609497)
COMMENTS: Cites: Toxicol Appl Pharmacol. 2007 Sep 15;223(3):288-98 (medline /17628626)
COMMENTS: Cites: EMBO J. 2007 Aug 8;26(15):3545-57 (medline /17641689)
COMMENTS: Cites: J Mol Biol. 2007 Sep 14;372(2):298-316 (medline /17663992)
COMMENTS: Cites: Hypertension. 2007 Nov;50(5):939-44 (medline /17785633)
COMMENTS: Cites: PPAR Res. 2009;2009:925309 (medline /20052392)
COMMENTS: Cites: Am J Physiol Endocrinol Metab. 2010 Sep;299(3):E335-40 (medline /20530738)
COMMENTS: Cites: PLoS One. 2011;6(1):e16344 (medline /21283829)
COMMENTS: Cites: Mol Endocrinol. 2011 Sep;25(9):1527-38 (medline /21835891)
COMMENTS: Cites: Mol Cell Endocrinol. 2010 Aug 30;325(1-2):54-63 (medline /20638986)
COMMENTS: Cites: J Biol Chem. 2000 Jun 16;275(24):18527-33 (medline /10748014)
COMMENTS: Cites: Biochem J. 2001 Jan 15;353(Pt 2):193-8 (medline /11139380)
COMMENTS: Cites: Mol Cell Biol. 2001 May;21(9):3057-70 (medline /11287611)
COMMENTS: Cites: Mol Endocrinol. 2002 May;16(5):1013-28 (medline /11981036)
COMMENTS: Cites: Bioinformatics. 2005 Jul 1;21(13):2933-42 (medline /15860560)
COMMENTS: Cites: J Biol Chem. 2005 Jul 15;280(28):26543-56 (medline /15888456)
COMMENTS: Cites: Hepatology. 2005 Aug;42(2):381-9 (medline /16025521)
COMMENTS: Cites: J Biol Chem. 2005 Sep 23;280(38):32565-8 (medline /16076839)
COMMENTS: Cites: DNA Cell Biol. 2005 Sep;24(9):582-94 (medline /16153159)
COMMENTS: Cites: Nucl Recept. 2005 Oct 3;3:3 (medline /16197558)
COMMENTS: Cites: Biotechniques. 2005 Nov;39(5):715-25 (medline /16315372)
COMMENTS: Cites: Curr Med Chem. 2005;12(25):2995-3009 (medline /16378501)
COMMENTS: Cites: Nucleic Acids Res. 2006 Jan 1;34(Database issue):D108-10 (medline /16381825)
COMMENTS: Cites: Nucleic Acids Res. 2006 Jan 1;34(Database issue):D632-6 (medline /16381948)
COMMENTS: Cites: Mol Cell Biochem. 2006 Jun;286(1-2):33-42 (medline /16534556)
COMMENTS: Cites: Nat Genet. 2006 Jun;38(6):626-35 (medline /16645617)
COMMENTS: Cites: Methods Mol Biol. 2010;585:147-58 (medline /19908002)
COMMENTS: Cites: Cell. 1992 Oct 2;71(1):73-85 (medline /1327537)
COMMENTS: Cites: Mol Endocrinol. 2002 Jun;16(6):1269-79 (medline /12040014)
COMMENTS: Cites: Mol Cell. 2003 Jan;11(1):139-50 (medline /12535528)
ABSTRACT: Human TNFAIP3 interacting protein 1 (TNIP1) has diverse functions including support of HIV replication through its interaction with viral Nef and matrix proteins, reduction of TNFα-induced signaling through its interaction with NF-κB pathway proteins, and corepression of agonist-bound retinoic acid receptors and peroxisome proliferator-activated receptors (PPAR). The wide tissue distribution of TNIP1 provides the opportunity to influence numerous cellular responses in these roles and defining control of TNIP1 expression would be central to improved understanding of its impact on cell function. We cloned 6kb of the human TNIP1 promoter and performed predictive and functional analyses to identify regulatory elements. The promoter region proximal to the transcription start site is GC-rich without a recognizable TATA box. In contrast to this proximal ~500bp region, 6kb of the promoter increased reporter construct constitutive activity over five-fold. Throughout the 6kb length, in silico analysis identified several potential binding sites for both constitutive and inducible transcription factors; among the latter were candidate NF-κB binding sequences and peroxisome proliferator response elements (PPREs). We tested NF-κB and PPAR regulation of the endogenous TNIP1 gene and cloned promoter by expression studies, electrophoretic mobility shift assays, and chromatin immunoprecipitations. We validated NF-κB sites in the TNIP1 promoter proximal and distal regions as well as one PPRE in the distal region. The ultimate control of the TNIP1 promoter is likely to be a combination of constitutive transcription factors and those subject to activation such as NF-κB and PPAR.
MESH HEADINGS: Base Sequence
MESH HEADINGS: Binding Sites
MESH HEADINGS: DNA-Binding Proteins/*genetics/metabolism
MESH HEADINGS: Gene Expression Regulation
MESH HEADINGS: HeLa Cells
MESH HEADINGS: Humans
MESH HEADINGS: Molecular Sequence Data
MESH HEADINGS: NF-kappa B/*genetics/metabolism
MESH HEADINGS: PPAR gamma/*genetics/metabolism
MESH HEADINGS: Peroxisome Proliferator-Activated Receptors/genetics/metabolism
MESH HEADINGS: *Promoter Regions, Genetic
MESH HEADINGS: Protein Binding/genetics
MESH HEADINGS: Regulatory Sequences, Nucleic Acid/*genetics
MESH HEADINGS: Response Elements/genetics
MESH HEADINGS: Signal Transduction
MESH HEADINGS: Transcription Factor RelA/genetics/metabolism
MESH HEADINGS: Transcription Initiation Site
MESH HEADINGS: Transcriptional Activation/genetics eng

509. Gururangan, S.; Chi, S. N.; Young Poussaint, T.; Onar-Thomas, A.; Gilbertson, R. J.; Vajapeyam, S.; Friedman, H. S.; Packer, R. J.; Rood, B. N.; Boyett, J. M., and Kun, L. E. Lack of Efficacy of Bevacizumab Plus Irinotecan in Children With Recurrent Malignant Glioma and Diffuse Brainstem Glioma: a Pediatric Brain Tumor Consortium Study.


Rec #: 50529
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: J Clin Oncol. 1999 May;17(5):1516-25 (medline /10334539)
COMMENTS: Cites: N Engl J Med. 1971 Nov 18;285(21):1182-6 (medline /4938153)
COMMENTS: Cites: Cancer Res. 2000 Apr 1;60(7):1878-86 (medline /10766175)
COMMENTS: Cites: Oncogene. 2000 Nov 20;19(49):5598-605 (medline /11114740)
COMMENTS: Cites: Cancer Cell. 2007 Jan;11(1):69-82 (medline /17222791)
COMMENTS: Cites: Cancer Cell. 2007 Jan;11(1):83-95 (medline /17222792)
COMMENTS: Cites: Clin Cancer Res. 2007 Feb 15;13(4):1253-9 (medline /17317837)
COMMENTS: Cites: Cancer. 2007 Oct 1;110(7):1542-50 (medline /17705175)
COMMENTS: Cites: Nat Rev Cancer. 2008 Apr;8(4):309-16 (medline /18337733)
COMMENTS: Cites: Neuro Oncol. 2008 Aug;10(4):624-30 (medline /18539884)
COMMENTS: Cites: Int J Radiat Oncol Biol Phys. 2008 Oct 1;72(2):383-9 (medline /18793954)
COMMENTS: Cites: Pediatr Blood Cancer. 2008 Dec;51(6):806-11 (medline /18802947)
COMMENTS: Cites: Clin Cancer Res. 2008 Oct 15;14(20):6371-5 (medline /18927275)
COMMENTS: Cites: J Neurooncol. 2009 Feb;91(3):329-36 (medline /18953493)
COMMENTS: Cites: J Clin Oncol. 2009 Feb 10;27(5):740-5 (medline /19114704)
COMMENTS: Cites: J Clin Oncol. 2009 Oct 1;27(28):4733-40 (medline /19720927)
COMMENTS: Cites: Cancer. 1993 Jul 1;72(1):271-5 (medline /8508417)
COMMENTS: Cites: Eur J Cancer. 2001 Nov;37(16):2064-72 (medline /11597385)
COMMENTS: Cites: NMR Biomed. 2002 Feb;15(1):6-17 (medline /11840548)
COMMENTS: Cites: J Neurooncol. 2002 Jul;58(3):237-53 (medline /12187958)
COMMENTS: Cites: J Clin Oncol. 2002 Dec 15;20(24):4684-91 (medline /12488414)
COMMENTS: Cites: J Clin Oncol. 2003 Sep 15;21(18):3542; author reply 3543 (medline /12972536)
COMMENTS: Cites: Am J Health Syst Pharm. 2004 Nov 1;61(21 Suppl 5):S21-6 (medline /15552623)
COMMENTS: Cites: J Natl Cancer Inst. 2005 Feb 2;97(3):172-87 (medline /15687360)
COMMENTS: Cites: Neurol Res. 2005 Jun;27(4):371-7 (medline /15949234)
COMMENTS: Cites: Blood. 2005 Oct 1;106(7):2347-55 (medline /15985545)
COMMENTS: Cites: Oncology. 2005;69 Suppl 3:25-33 (medline /16301833)
COMMENTS: Cites: Cancer. 2006 Mar 15;106(6):1364-71 (medline /16463390)
COMMENTS: Cites: J Natl Cancer Inst. 1990 Jan 3;82(1):4-6 (medline /1688381)
COMMENTS: Cites: J Clin Oncol. 1990 Jul;8(7):1277-80 (medline /2358840)
COMMENTS: Cites: J Neurooncol. 1999 May;43(1):43-7 (medline /10448870)
ABSTRACT: PURPOSE: A phase II study of bevacizumab (BVZ) plus irinotecan (CPT-11) was conducted in children with recurrent malignant glioma (MG) and intrinsic brainstem glioma (BSG).
ABSTRACT: PATIENTS AND METHODS: Eligible patients received two doses of BVZ intravenously (10 mg/kg) 2 weeks apart and then BVZ plus CPT-11 every 2 weeks until progressive disease, unacceptable toxicity, or a maximum of 2 years of therapy. Correlative studies included diffusion weighted and T1 dynamic contrast-enhanced permeability imaging, BVZ pharmacokinetics, and estimation of vascular endothelial growth factor receptor 2 (VEGFR-2) phosphorylation in peripheral blood mononuclear cells (PBMC) after single-agent BVZ.
ABSTRACT: RESULTS: Thirty-one evaluable patients received a median of two courses of BVZ plus CPT-11 (range, 1 to 19). No sustained responses were observed in either stratum. Median time to progression for all 34 eligible patients enrolled was 127 days for MG and 71 days for BSG. Progression-free survival rates at 6 months were 41.8% and 9.7% for MG and BSG, respectively. Toxicities related to BVZ included grade 1 to 3 fatigue in seven patients, grade 1 to 2 hypertension in seven patients, grade 1 CNS hemorrhage in four patients, and grade 4 CNS ischemia in two patients. The mean diffusion ratio decreased after two doses of BVZ in patients with MG only. Vascular permeability parameters did not change significantly after therapy in either stratum. Inhibition of VEGFR-2 phosphorylation in PBMC was detected in eight of 11 patients after BVZ exposure.
ABSTRACT: CONCLUSION: BVZ plus CPT-11 was well-tolerated but had minimal efficacy in children with recurrent malignant glioma and brainstem glioma.
MESH HEADINGS: Adolescent
MESH HEADINGS: Adult
MESH HEADINGS: Antibodies, Monoclonal/administration &
MESH HEADINGS: dosage
MESH HEADINGS: Antibodies, Monoclonal, Humanized
MESH HEADINGS: Antineoplastic Combined Chemotherapy Protocols/*therapeutic use
MESH HEADINGS: Brain Neoplasms/*drug therapy/metabolism/pathology
MESH HEADINGS: Brain Stem Neoplasms/*drug therapy/metabolism/pathology
MESH HEADINGS: Camptothecin/administration &
MESH HEADINGS: dosage/analogs &
MESH HEADINGS: derivatives
MESH HEADINGS: Child
MESH HEADINGS: Diffusion Magnetic Resonance Imaging
MESH HEADINGS: Glioma/*drug therapy/metabolism/pathology
MESH HEADINGS: Humans
MESH HEADINGS: Neoplasm Recurrence, Local/*drug therapy/metabolism/pathology
MESH HEADINGS: Phosphorylation
MESH HEADINGS: Survival Rate
MESH HEADINGS: Treatment Outcome
MESH HEADINGS: Vascular Endothelial Growth Factor Receptor-2/metabolism
MESH HEADINGS: Young Adult eng

510. Guyton, K. Z.; Chiu, W. A.; Bateson, T. F.; Jinot, J.; Scott, C. S.; Brown, R. C., and Caldwell, J. C. A Reexamination of the Ppar-Alpha Activation Mode of Action as a Basis for Assessing Human Cancer Risks of Environmental Contaminants.


Rec #: 50719
Keywords: NO TOXICANT
Notes: Chemical of Concern: CPY
Abstract: ABSTRACT: BACKGROUND: Diverse environmental contaminants, including the plasticizer di(2-ethylhexyl)phthalate (DEHP), are hepatocarcinogenic peroxisome proliferators in rodents. Peroxisome proliferator-activated receptor-alpha (PPAR-alpha) activation and its sequelae have been proposed to constitute a mode of action (MOA) for hepatocarcinogenesis by such agents as a sole causative factor. Further, based on a hypothesized lower sensitivity of humans to this MOA, prior reviews have concluded that rodent hepatocarcinogenesis by PPAR-alpha agonists is irrelevant to human carcinogenic risk.
ABSTRACT: DATA SYNTHESIS: Herein,
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