Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency.

Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency. Research Abstract Details 

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Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency. Abstract Text:

Gennaro Giordano,Zhara Afsharinejad,Marina Guizzetti,Annabella Vitalone,Terrance J Kavanagh,Lucio G Costa,

Over the past several years evidence has been accumulating from in vivo animal studies, observations in humans, and in vitro studies, that organophosphorus (OP) insecticides may induce oxidative stress. Such effects may contribute to some of the toxic manifestations of OPs, particularly upon chronic or developmental exposures. The aim of this study was to investigate the role of oxidative stress in the neurotoxicity of two commonly used OPs, chlorpyrifos (CPF) and diazinon (DZ), their oxygen analogs (CPO and DZO), and their "inactive" metabolites (TCP and IMP), in neuronal cells from a genetic model of glutathione deficiency. Cerebellar granule neurons from wild type mice (Gclm +/+) and mice lacking the modifier subunit of glutamate cysteine ligase (Gclm -/-), the first and limiting step in the synthesis of glutathione (GSH), were utilized. The latter display very low levels of GSH and are more susceptible to the toxicity of agents that increase oxidative stress. CPO and DZO were the most cytotoxic compounds, followed by CPF and DZ, while TCP and IMP displayed lower toxicity. Toxicity was significantly higher (10- to 25-fold) in neurons from Gclm (-/-) mice, and was antagonized by various antioxidants. Depletion of GSH from Gclm (+/+) neurons significantly increased their sensitivity to OP toxicity. OPs increased intracellular levels of reactive oxygen species and lipid peroxidation and in both cases the effects were greater in neurons from Gclm (-/-) mice. OPs did not alter intracellular levels of GSH, but significantly increased those of oxidized glutathione (GSSG). Cytotoxicity was not antagonized by cholinergic antagonists, but was decreased by the calcium chelator BAPTA-AM. These studies indicate that cytotoxicity of OPs involves generation of reactive oxygen species and is modulated by intracellular GSH, and suggest that it may involve disturbances in intracellular homeostasis of calcium.

Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency. Publishing Authors By Initials

G Giordano,Z Afsharinejad,M Guizzetti,A Vitalone,TJ Kavanagh,LG Costa,

For similar inorganic chemicals: free radicals: reactive oxygen species research abstracts see: inorganic chemicals: free radicals: reactive oxygen species research

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Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Toxicology and applied pharmacology

VOLUME: 219

Page Numbers: 181-9

Journal Abbreviation: Toxicol. Appl. Pharmacol.

ISSN: 0041-008X

DAY: 4

MONTH: 10

YEAR: 2006

Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 416575

Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency. Keywords Mesh Terms:

KEYWORDS: Reactive Oxygen Species

MESH TERMS: metabolism

Chemical & Substance for Abstract: Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency. Information

Substance Name: Glutathione

Registry Number: 70-18-8

Grant and Affiliation Information for Organophosphorus insecticides chlorpyrifos and diazinon and oxidative stress in neuronal cells in a genetic model of glutathione deficiency.

AFFILIATION: Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98105, USA.

Country: United States

AGENCY: United States NIEHS

GRANT: P30ES07033

ACRONYM: ES

MEDLINETA: Toxicol Appl Pharmacol

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