Trichlorfon-induced apoptosis in hepatocyte primary cultures of Carassius auratus gibelio.

Trichlorfon, an organophosphorus pesticide, can disrupt metabolism, reproduction and immune functions of some aquatic animals. In the present study, the effect of trichlorfon on apoptosis and the underlying apoptotic mechanism were investigated in primary cultures of Carassius auratus gibelio hepatocytes. Analyses of cultures exposed to 0, 0.01, 0.1, and 1.0 mg L(-1) trichlorfon concentrations for 24h indicated that trichlorfon induced apoptosis and caused nuclear shrinkage, cell membrane rupture, cytoskeletal collapse, loss of cytoplasm, mitochondria vacuolization, and apoptotic body formation, as well as lipid droplet accumulation. Trichlorfon increased intracellular reactive oxygen species and malondialdehyde concentrations and caused cytochrome c release from mitochondria into the cytoplasm, leading to caspase-3 activation. These findings contributed to a better understanding of the mechanisms underlying trichlorfon-induced apoptosis via activation of mitochondrial pathways while clearly indicating that trichlorfon-induced cell death was via apoptosis accompanied by mitochondrial cytochrome c release and consequent caspase-3 activation.