Abstract
The organochlorine cyclodiene insecticide, endosulfan readily penetrates into the brain. The neurotoxic action of endosulfan has been attributed to its α-isomer. Endosulfan sulphate which is a chief metabolite of endosulfan seems to contribute to its acute neurotoxic action which is manifested by clonic convulsions in experimental animals. Convulsant and proconvulsant effects of endosulfan are apparent after its chronic exposure at low dose levels. These effects have been attributed to its γ-aminobutyric acid antagonistic action. Repeated exposure to low doses has resulted in behavioral changes too. Endosulfan-induced hyper-excitability has been associated with its muscarinic receptor stimulating action. The insecticide has been shown to produce aggressive behaviour and learning impairment by activating serotonergic mechanism. A dopaminergic involvement has been suggested for endosulfan-induced hypermotoractivity and circling movement. Animals exposed chronically to low doses of the insecticide have responded more markedly than control animals to the pharmacological actions of diazepam, chlorpromazine, pentobarbital and ethanol. The findings reviewed here emphasize awareness that chronic occupational exposure to low doses of endosulfan may result not only in behavioral abberations but in hazardous interaction with centrally acting drugs too.
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