Heptachlor induced mitochondria-mediated cell death via impairing electron transport chain complex III

•Heptachlor inhibited mitochondrial electron transport chain complex III activity.•Heptachlor promoted generation of reactive oxygen species.•Heptachlor induced Bax activation.•Heptachlor induced mitochondria-mediated and caspase-dependent apoptosis. Environmental toxins like pesticides have been implicated in the pathogenesis of Parkinson’s disease (PD). Epidemiological studies suggested that exposures to organochlorine pesticides have an association with an increased PD risk. In the present study, we examined the mechanism of toxicity induced by an organochlorine pesticide heptachlor. In a human dopaminergic neuroblastoma SH-SY5Y cells, heptachlor induced both morphological and functional damages in mitochondria. Interestingly, the compound inhibited mitochondrial electron transport chain complex III activity. Rapid generation of reactive oxygen species and the activation of Bax were then detected. Subsequently, mitochondria-mediated, caspase-dependent apoptosis followed. Our results raise a possibility that an organochlorine pesticide heptachlor can act as a neurotoxicant associated with PD.