Appendix 2-5: Rejected ecotox bibliography for Chlorpyrifos



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using available data on the acute sensitivity and toxicokinetics of a range of freshwater arthropods exposed to chlorpyrifos. The results of a quantitative linking of seven different endpoints and twelve traits demonstrate that while quantitative links between traits and/or trait combinations and process based (toxicokinetic) model parameters can be established, the use of simple traits to predict classical sensitivity endpoints yields little insight. Remarkably, neither of the standard sensitivity values, i.e. the LC sub(50) or EC sub(50), showed a strong correlation with traits. Future research in this area should include a quantitative linking of toxicodynamic parameter estimations and physiological traits, and requires further consideration of how mechanistic trait-process/parameter links can be used for prediction of intrinsic sensitivity across species for different substances in ERA.
Keywords: Risk assessment
Keywords: Data processing
Keywords: Toxicants
Keywords: Ecology Abstracts; Toxicology Abstracts; Pollution Abstracts
Keywords: Freshwater environments
Keywords: Environmental Studies
Keywords: Models
Keywords: Chlorpyrifos
Keywords: Arthropoda
Keywords: Insecticides
Keywords: Structure-function relationships
Keywords: Invertebrata
Keywords: X 24330:Agrochemicals
Date revised - 2012-09-01
Language of summary - English
Pages - 2088-2101
ProQuest ID - 1143779992
SubjectsTermNotLitGenreText - Risk assessment; Chlorpyrifos; Insecticides; Data processing; Toxicants; Freshwater environments; Structure-function relationships; Models; Arthropoda; Invertebrata
Last updated - 2012-11-09
Corporate institution author - Rubach, Mascha N; Baird, Donald J; Boerwinkel, Marie-Claire; Maund, Stephen J; Roessink, Ivo; Brink, Paul J
DOI - OB-19d531ea-9c48-4906-bffamfgefd107; 17187658; 0963-9292; 1573-3017 English

1155. Rudzok, S; Schmucking, E; Graebsch, C; Herbarth, O; Bauer, M, and Rudzok, S. The Inducibility of Human Cytochrome P450 1a by Environmental-Relevant Xenobiotics in the Human Hepatoma Derived Cell Line Hepg2. 2009 Nov; 28, (3): 370-378.


Rec #: 44539
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: Overexpression of the CYP1 family, independent of gender, is focal to the evaluation of the risk of human cancer. We have analysed the ability of 17 anthropogenic environmental xenobiotics widely used in Europe within households and agriculture to induce the human cytochrome P450 1A (CYP1A) in the human hepatoma derived cell line HepG2. The xenobiotics were potent to concomitantly induce both CYP1A mRNA and CYP1A activity in a dose-response relationship. Exceptions were shown by the organophosphate insecticide chlorpyrifos and the imidazole fungicide prochloraz in high concentrations which were capable of both inhibiting the basal or abolishing the initially induced CYP1A activity, respectively. A CYP1A induction has been shown for the first time by the aromatic xenobiotics irgasan, permethrin and azoxystrobin, the nonaromatic tributyltinoxide and for humans by the piperonylbutoxide. The xenobiotics additionally differed by their induced CYP1A isoenzyme pattern. A pronounced CYP1A1 and CYP1A2 mRNA induction was given by the phenyl urea herbicide diuron and benzodiazole insecticide piperonylbutoxide, respectively. In conclusion, out of the environmental xenobiotics, we described new members of human CYP1A inducers which extend chemical structures of biotransformation activators.
Keywords: Agriculture
Keywords: imidazole
Keywords: Organophosphates
Keywords: biotransformation
Keywords: Urea
Keywords: diuron
Keywords: Europe
Keywords: Xenobiotics
Keywords: azoxystrobin
Keywords: Hepatoma
Keywords: Prochloraz
Keywords: Insecticides
Keywords: Toxicology Abstracts; Environment Abstracts
Keywords: Dose-response effects
Keywords: Isoenzymes
Keywords: X 24330:Agrochemicals
Keywords: CYP1A2 protein
Keywords: Diuron
Keywords: Permethrin
Keywords: Herbicides
Keywords: organophosphates
Keywords: Cancer
Keywords: ENA 02:Toxicology & Environmental Safety
Keywords: mRNA
Keywords: Chlorpyrifos
Keywords: Cytochrome
Keywords: CYP1A protein
Keywords: Fungicides
Keywords: Cytochrome P450
Keywords: Aromatics
Date revised - 2009-10-01
Language of summary - English
Location - Europe
Pages - 370-378
ProQuest ID - 20944792
SubjectsTermNotLitGenreText - Agriculture; imidazole; CYP1A2 protein; Diuron; biotransformation; Permethrin; Herbicides; Urea; organophosphates; Xenobiotics; Cancer; mRNA; azoxystrobin; Chlorpyrifos; Hepatoma; Prochloraz; CYP1A protein; Insecticides; Dose-response effects; Fungicides; Isoenzymes; Cytochrome P450; Aromatics; Cytochrome; Organophosphates; diuron; Europe
Last updated - 2011-12-14
British nursing index edition - Environmental Toxicology and Pharmacology [Environ. Toxicol. Pharmacol.]. Vol. 28, no. 3, pp. 370-378. Nov 2009.
Corporate institution author - Rudzok, S; Schmucking, E; Graebsch, C; Herbarth, O; Bauer, M
DOI - MD-0010595319; 11034675; 1382-6689 English

1156. Ruggenenti, P.; Fassi, A.; Ilieva, A.; Iliev, I. P.; Chiurchiu, C.; Rubis, N.; Gherardi, G.; Ene-Iordache, B.; Gaspari, F.; Perna, A.; Cravedi, P.; Bossi, A.; Trevisan, R.; Motterlini, N.; Remuzzi, G., and Benedict-B Study Investigators. Effects of Verapamil Added-on Trandolapril Therapy in Hypertensive Type 2 Diabetes Patients With Microalbuminuria: the Benedict-B Randomized Trial.


Rec #: 50309
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: ABSTRACT: OBJECTIVES: To address whether nondihydropyridine calcium-channel blocker added-on angiotensin-converting-enzyme inhibitor therapy ameliorates albuminuria and cardiovascular outcomes in type 2 diabetes patients.
ABSTRACT: DESIGN: The Bergamo Nephrologic Diabetes Complications Trial-B was a multicentre, prospective, double-blind, parallel-group trial comparing renal and cardiovascular outcomes in 281 hypertensive type 2 diabetes patients with microalbuminuria randomized to at least 2-year VeraTran (verapamil/trandolapril 180 mg/2 mg daily) or trandolapril (2 mg daily, identical image) treatment. Main outcome was persistent macroalbuminuria (albuminuria >200 µg/min in two consecutive visits). Treatment targets were SBP/DBP less than 120/80 mmHg and HbA1C less than 7%.
ABSTRACT: RESULTS: Over a median follow-up of 4.5 years, 18 patients (13%) on VeraTran vs. 15 (10.5%) on trandolapril [unadjusted hazard ratio (95% confidence interval [CI]) 1.07 (0.54-2.12), P = 0.852] progressed to macroalbuminuria, respectively; 62 (44.9%) vs. 71 (49.7%) [0.80 (0.57-1.12), P = 0.198] regressed to normoalbuminuria (urinary albumin excretion < 20 µg/min), and 20 (14.5%) vs. 21 (14.7%) [hazard ratio 0.93 (0.50-1.72), P = 0.816] had major cardiovascular events. BP and metabolic control were similar between groups. Patients with cardiovascular events were significantly less [13 (9.8%) vs. 28 (18.9%), hazard ratio: 0.37 (0.19-0.71), P = 0.003] among those regressing to normoalbuminuria than those without regression. Difference was independent of treatment allocation and was significant also after adjusting for baseline characteristics [0.40 (0.20-0.79), P = 0.009], follow-up SBP [0.40 (0.20-0.80), P = 0.010] or DBP [0.36 (0.18-0.73), P = 0.004] BP or HbA1C [0.43 (0.21-0.88), P = 0.021].
ABSTRACT: CONCLUSION: In hypertensive type 2 diabetes patients with microalbuminuria, verapamil added-on trandolapril did not improve renal or cardiovascular outcomes. Independent of verapamil, trandolapril normalized albuminuria in half of patients and this translated into significant cardioprotection.
MESH HEADINGS: Aged
MESH HEADINGS: Albuminuria/*complications/*drug therapy
MESH HEADINGS: Angiotensin-Converting Enzyme Inhibitors/administration &
MESH HEADINGS: dosage
MESH HEADINGS: Antihypertensive Agents/*administration &
MESH HEADINGS: dosage/adverse effects
MESH HEADINGS: Calcium Channel Blockers/administration &
MESH HEADINGS: dosage
MESH HEADINGS: Cardiovascular Diseases/prevention &
MESH HEADINGS: control
MESH HEADINGS: Diabetes Mellitus, Type 2/*complications/*drug therapy
MESH HEADINGS: Double-Blind Method
MESH HEADINGS: Female
MESH HEADINGS: Humans
MESH HEADINGS: Hypertension/*complications/*drug therapy
MESH HEADINGS: Indoles/*administration &
MESH HEADINGS: dosage
MESH HEADINGS: Male
MESH HEADINGS: Middle Aged
MESH HEADINGS: Prospective Studies
MESH HEADINGS: Treatment Outcome
MESH HEADINGS: Verapamil/*administration &
MESH HEADINGS: dosage eng

1157. Rush, T; Liu, X Q; Hjelmhaug, J, and Lobner, D. Mechanisms of Chlorpyrifos and Diazinon Induced Neurotoxicity in Cortical Culture. 2010 Mar 31; 166, (3): 899-906.


Rec #: 40669
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: The main action of organophosphorous insecticides is generally believed to be the inhibition of acetylcholinesterase (AChE). However, these compounds also inhibit many other enzymes, any of which may play a role in their toxicity. We tested the neurotoxic mechanism of two organophosphorous insecticides, chlorpyrifos and diazinon in primary cortical cultures. Exposure to the insecticides caused a concentration-dependent toxicity that could not be directly attributed to the oxon forms of the compounds which caused little toxicity but strongly inhibited AChE. Addition of 1 mM acetylcholine or carbachol actually attenuated the toxicity of chlorpyrifos and diazinon, and the muscarinic receptor antagonist, atropine, and the nicotinic receptor antagonist, mecamylamine, did not attenuate the toxicity of either insecticide. These results strongly suggest that the organophosphorous toxicity observed in this culture system is not mediated by buildup of extracellular acetylcholine resulting from inhibition of AChE. The toxicity of chlorpyrifos was attenuated by antagonists of either the NMDA or AMPA/kainate-type glutamate receptors, but the cell death was potentiated by the caspase inhibitor ZVAD. Diazinon toxicity was not affected by glutamate receptor antagonists, but was attenuated by ZVAD. Chlorpyrifos induced diffuse nuclear staining characteristic of necrosis, while diazinon induced chromatin condensation characteristic of apoptosis. Also, chlorpyrifos exposure increased the levels of extracellular glutamate, while diazinon did not. The results suggest two different mechanisms of neurotoxicity of the insecticides, neither one of which involved acetylcholine. Chlorpyrifos induced a glutamate-mediated excitotoxicity, while diazinon induced apoptotic neuronal death. Copyright 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
Keywords: 2921-88-2
Keywords: Cerebral Cortex -- cytology
Keywords: Animals
Keywords: Cerebral Cortex -- drug effects
Keywords: Apoptosis
Keywords: Cerebral Cortex -- metabolism
Keywords: Acetylcholinesterase
Keywords: Receptors, Kainic Acid -- physiology
Keywords: Caspase Inhibitors
Keywords: Acetylcholine -- metabolism
Keywords: Receptors, N-Methyl-D-Aspartate -- physiology
Keywords: Necrosis
Keywords: Insecticides
Keywords: Cholinesterase Inhibitors -- toxicity
Keywords: Acetylcholinesterase -- metabolism
Keywords: 333-41-5
Keywords: Receptors, Kainic Acid
Keywords: Extracellular Space -- enzymology
Keywords: EC 3.1.1.7
Keywords: Receptors, N-Methyl-D-Aspartate
Keywords: 51-84-3
Keywords: Insecticides -- toxicity
Keywords: Diazinon -- toxicity
Keywords: benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
Keywords: Mice
Keywords: Chlorpyrifos
Keywords: Cholinesterase Inhibitors
Keywords: 0
Keywords: Chlorpyrifos -- toxicity
Keywords: Cells, Cultured
Keywords: Amino Acid Chloromethyl Ketones
Keywords: Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors
Keywords: Acetylcholine
Keywords: Receptors, Kainic Acid -- antagonists & inhibitors
Keywords: Amino Acid Chloromethyl Ketones -- pharmacology
Keywords: Diazinon
Date completed - 2010-05-17
Date created - 2010-03-11
Date revised - 2012-12-20
Language of summary - English
Pages - 899-906
ProQuest ID - 733525226
Last updated - 2013-01-19
British nursing index edition - Neuroscience, March 31, 2010, 166(3):899-906
Corporate institution author - Rush, T; Liu, X Q; Hjelmhaug, J; Lobner, D
DOI - MEDL-20096330; 20096330; 1873-7544 eng

1158. Rush, Travis and Lobner, Doug. Mechanisms of Neuronal Death Induced by Environmental Toxicants in Murine Cortical Culture. 2011: (UMI# 3478356 ).


Rec #: 51669
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: This study was directed at examining the neurotoxic mechanisms of several classes of environmental toxicants implicated in neurodegenerative disease. Primary cortical cultures were exposed to organophosphorus pesticides, heavy metals and the cyanobacterial toxin, beta-N-methylamino-L-alanine (BMAA). Several components relating to neuronal injury were assessed in each study and novel aspects are described. The main action of organophosphorous insecticides is generally believed to be the inhibition of acetylcholinesterase. However, these compounds are now recognized to inhibit many other enzymes and cause neuronal death through a variety of mechanisms. I found that exposure to chlorpyrifos or diazinon caused concentration-dependent neurotoxicity that could not be attributed to acetylcholinesterase inhibition. Chlorpyrifos exposure increased extracellular glutamate and induced a diffuse nuclear staining characteristic of necrosis; the toxicity was sensitive to ionotropic glutamate receptor antagonists. Diazinon toxicity was blocked by caspase inhibitors. Additionally, diazinon induced punctuate chromatin staining characteristic of apoptosis. These results represent two distinct, novel mechanisms of organophosphorous neurotoxicity. Heavy metals are ubiquitous in the environment and are of significant health concern worldwide. Exposure to lead, iron, mercurials (inorganic mercury, methylmercury, or thimerosal, i.e. ethylmercury) or other heavy metals is implicated as a risk factor for neurodegenerative disease. I found that the toxicity of these metals may be enhanced when interacting with chelators used to treat metal intoxication. As well, my studies describe a new role for mercury-induced oxidative stress as a cytoprotective signal to enhance glutathione levels. My data also suggests an obligate role for MRP1 in the detoxification of methylmercury. Neurodegenerative diseases likely involve complex interactions between genetic predisposition and multiple environmental factors. My final study tested the interaction of the methylmercury and BMAA. Importantly, concentrations of BMAA that caused no toxicity by themselves potentiated methyl mercury toxicity. BMAA plus methylmercury, at concentrations that had no effect by themselves, depleted cellular glutathione. The combined toxicity was attenuated by glutathione monoethyl ester, and the free radical scavenger, trolox, but not by the NMDA receptor antagonist, MK-801. The results indicate a synergistic neurotoxic interaction targeting the cellular redox state. This finding may have implications for neurodegenerative disease caused by environmental toxicant exposure.
Start Page: 140
ISSN/ISBN: 9781124958026
Keywords: 0383:Surgery
Keywords: Methylmercury
Keywords: Toxicants
Keywords: Neuronal death
Keywords: Glutathione
Keywords: Pesticides
Keywords: 0383:Toxicology
Keywords: Health and environmental sciences
Keywords: Neurodegeneration
Keywords: Biological sciences
Keywords: 0317:Neurosciences
Methylmercury
Neuronal death
Toxicants
Glutathione
57703061
Rush, Travis
2011-11-14
0383: Toxicology
66569
0383: Surgery
Neurodegeneration
n/a
English
0317: Neurosciences
Pesticides
Copyright ProQuest, UMI Dissertations Publishing 2011
902628276
2011
3478356
Health and environmental sciences
9781124958026
Biological sciences
2505623611 English

1159. Rutschmann, S. and Hoebe, K. Dissecting Innate Immunity by Germline Mutagenesis.


Rec #: 51319
Keywords: NO TOXICANT
Notes: Chemical of Concern: CPY
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ABSTRACT: The innate arm of our immune system is the first line of defence against infections. In addition, it is believed to drive adaptive immune responses, which help fight pathogens and provide long-term memory. As such, the innate immune system is instrumental for protection against pathogens that would otherwise destroy their host. Although our understanding of the innate immune components involved in pathogen sensing and fighting is improving, it is still limited. This is particularly exemplified by increased documentation of innate immune deficiencies in humans that often result in high and recurrent susceptibility to infections or even death, without the genetic cause being evident. To provide further insight into the mechanisms by which pathogen sensing and eradication occur, several strategies can be used.
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