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• W2960483150 abstract "• Organophosphate and N-methyl carbamate pesticides are identified as two common mechanism groups in cumulative risk assessment. • We apply QSAR-, cell-, and small organism-based new approach methodologies (NAMs) to examine their mechanisms of action. • In some cases, mitochondrial toxicity of organophosphate pesticides may augment the disruption of acetylcholine signaling in developmental toxicity. • This study provides a proof of concept for applying NAMs to refine the existing groups based on dissimilar mechanisms of action. • NAMs are also useful to define new common mechanism groups based on structural features. Mitochondrial toxicity has been proposed as a potential cause of developmental defects in humans. We evaluated 51 organophosphate and carbamate pesticides using the U.S. EPA ToxCast and Tox21 databases. Only a small number of them bind directly to cholinesterases in the parent form. The hydrophobicity of organophosphate pesticides is correlated significantly to TSPO binding affinity, mitochondrial membrane potential reduction in HepG2 cells, and developmental toxicity in Caenorhabditis elegans and Danio rerio ( p < 0.05). Structural analysis suggests that in some cases the Krebs cycle is a potential target of organophosphate and carbamate exposure at early life stages. The results support the hypothesis that mitochondrial effects of some organophosphate pesticides—particularly those that require enzymatic activation to the oxon form—may augment the documented effects of disruption of acetylcholine signaling. This study provides a proof of concept for applying new approach methodologies to interrogate mechanisms of action for cumulative risk assessment." @default.
• W2960483150 created "2019-07-23" @default.
• W2960483150 creator A5015141183 @default.
• W2960483150 creator A5044754192 @default.
• W2960483150 date "2019-10-01" @default.
• W2960483150 modified "2023-10-16" @default.
• W2960483150 title "Mitochondria as a target of organophosphate and carbamate pesticides: Revisiting common mechanisms of action with new approach methodologies" @default.
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• W2960483150 doi "https://doi.org/10.1016/j.reprotox.2019.07.007" @default.
• W2960483150 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6766410" @default.
• W2960483150 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31315019" @default.
• W2960483150 hasPublicationYear "2019" @default.
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