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[Neurotoxicity of organophosphorus and dithiocarbamate compounds]
1Department of Public Health, Fukushima Medical University, School of Medicine, 1 Hikarigaoka, Fukushima 960-1295, Japan.
Abstract:
The neurotoxicity of organophosphorus compounds (OPs) including leptophos, TOCP and triphenyl phosphite and dithiocarbamate compounds were reviewed in this study. The major neurotoxicities of OPs were acute toxicity produced by the acetylcholine esterase (AChE) inhibiting action of OPs and delayed neurotoxicity produced by such OPs as leptophos and TOCP. The direct action of OP on the muscarinic and/or nicotinic acethylcholine receptors in the synaptic membranes have lately attracted attention in relation to acute toxicity. Delayed neurotoxicity is a delayed onset of prolonged locomotor ataxia resulting from a single or repeated exposure to an OP. Although neurotoxic esterase (NTE) inhibition might be related to the onset of organophosphate-induced delayed neurotoxicity (OPIDN), the precise mode of action is not yet clear. The effect of dithiocarbamates on the nervous system is also mentioned, because the compounds are currently suspected not only for neurotoxicity, but also as endocrine-disrupting chemicals. Although dithiocarbamates showed weak neurotoxicity in adult animals, we need to pay more attention to developmental neurotoxicity.
Insights
Organophosphorus compounds (OPs) cause acute toxicity by inhibiting acetylcholine esterase (AChE) and delayed neurotoxicity. Dithiocarbamates also show neurotoxic potential, especially in development.
Area of Science:
- Neuroscience
- Toxicology
- Environmental Health
Context:
- Organophosphorus compounds (OPs) are widely used pesticides and industrial chemicals.
- Neurotoxicity is a significant concern associated with exposure to OPs and dithiocarbamates.
- Understanding the mechanisms of neurotoxicity is crucial for risk assessment and mitigation.
Purpose:
- To review the neurotoxic effects of organophosphorus compounds (OPs) and dithiocarbamates.
- To elucidate the mechanisms underlying acute and delayed neurotoxicity induced by OPs.
- To highlight the potential neurotoxic and endocrine-disrupting effects of dithiocarbamates.
Summary:
- OPs induce acute neurotoxicity via acetylcholine esterase (AChE) inhibition and delayed neurotoxicity (OPIDN), potentially involving neurotoxic esterase (NTE) inhibition.
- Leptophos and TOCP are examples of OPs causing delayed neurotoxicity, characterized by locomotor ataxia.
- Dithiocarbamates exhibit weak neurotoxicity in adults but warrant attention for developmental neurotoxicity and endocrine disruption.
Impact:
- Informs the assessment of risks associated with OP and dithiocarbamate exposure.
- Highlights the need for further research into the precise mechanisms of OPIDN.
- Emphasizes the importance of considering developmental neurotoxicity for dithiocarbamates.