The Effect of Organophosphate Exposure on Neuronal Cell Coenzyme Q 10 Status

Organophosphate (OP) compounds are widely used as pesticides and herbicides and exposure to these compounds has been associated with both chronic and acute forms of neurological dysfunction including cognitive impairment, neurophysiological problems and cerebral ataxia with evidence of mitochondrial...

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Bibliographic Details
Published in:Neurochemical research 2021-01, Vol.46 (1), p.131
Main Authors: Turton, Nadia, Heaton, Robert A, Ismail, Fahima, Roberts, Sioned, Nelder, Sian, Phillips, Sue, Hargreaves, Iain P
Format: Article
Language:English
Subjects:
Cell Line, Tumor
Cell Survival - drug effects
Chlorpyrifos - toxicity
Dichlorvos - toxicity
Electron Transport Complex II - metabolism
Electron Transport Complex III - metabolism
Humans
Insecticides - toxicity
Methyl Parathion - toxicity
Mitochondria - drug effects
Neurons - drug effects
Ubiquinone - analogs & derivatives
Ubiquinone - metabolism
Ubiquinone - pharmacology
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Summary:Organophosphate (OP) compounds are widely used as pesticides and herbicides and exposure to these compounds has been associated with both chronic and acute forms of neurological dysfunction including cognitive impairment, neurophysiological problems and cerebral ataxia with evidence of mitochondrial impairment being associated with this toxicity. In view of the potential mitochondrial impairment, the present study aimed to investigate the effect of exposure to commonly used OPs, dichlorvos, methyl-parathion (parathion) and chloropyrifos (CPF) on the cellular level of the mitochondrial electron transport chain (ETC) electron carrier, coenzyme Q (CoQ ) in human neuroblastoma SH-SY5Y cells. The effect of a perturbation in CoQ status was also evaluated on mitochondrial function and cell viability. A significant decreased (P 
ISSN:1573-6903