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Neurotoxic actions of pyrethroid insecticides
D M Soderlund1, J R Bloomquist
1Department of Entomology, Cornell University, Geneva, New York 14456.
Annual Review of Entomology
|January 1, 1989
Summary
Pyrethroid insecticides primarily target voltage-sensitive sodium channels in insects and mammals. While these channels are the main site of action, other channels and receptors may also contribute to pyrethroid toxicity.
Area of Science:
- Neuroscience
- Toxicology
- Molecular Biology
Background:
- Pyrethroid insecticides are widely used neurotoxic agents.
- Their precise molecular targets and mechanisms of action are complex and multifaceted.
Purpose of the Study:
- To elucidate the principal molecular target site of pyrethroids.
- To differentiate the actions of Type I and Type II pyrethroids.
- To explore additional sites of action beyond the primary target.
Main Methods:
- Biophysical and biochemical studies of sodium channel function.
- In vivo assessments of neurotoxicity and poisoning syndromes.
- Investigation of effects on insect neurosecretory neurons and mammalian neurotransmitter release.
Main Results:
- Evidence strongly implicates voltage-sensitive sodium channels as the primary target for all pyrethroids and DDT analogs.
- Type I and Type II pyrethroids exhibit distinct effects on sodium channel kinetics and neuronal excitability.
- Pyrethroids may also affect voltage-sensitive calcium channels and peripheral-type benzodiazepine receptors, contributing to intoxication.
Conclusions:
- The voltage-sensitive sodium channel is the principal molecular target for pyrethroids.
- Qualitatively different effects on sodium channels explain distinct poisoning syndromes.
- Additional targets, including calcium channels and benzodiazepine receptors, may contribute to pyrethroid toxicity.