Long-term toxicity of lindane through oxidative stress and cell apoptosis in Caenorhabditis elegans.

Abstract

Lindane persists in the environment and bioaccumulates as an organochlorine pesticide and can pose risks to ecological environments and human health. To explore the long-term toxicity and underlying mechanisms of lindane, Caenorhabditis elegans was chosen as an animal model for toxicological study. The indicators of physiological, oxidative stress and cell apoptosis were examined in nematodes chronically exposed to environmentally relevant concentrations of lindane (0.01-100ng/L). The data suggested that exposure to lindane at doses above 0.01ng/L induced adverse physiological effects in C.elegans. Significant increases of ROS production and lipofuscin accumulation were observed in 100ng/L of lindane-exposed nematodes, suggesting that lindane exposure induced oxidative stress in nematodes. Exposure to 10-100ng/L of lindane also significantly increased the average number of germ cell corpses, which indicated cell apoptosis induced by lindane in C.elegans. Moreover, chronic exposure to 100ng/L lindane significantly influenced the expression of genes related to oxidative stress and cell apoptosis (e.g., isp-1, sod-3, ced-3, and cep-1 genes). These results indicated that oxidative stress and cell apoptosis could play an important role in toxicity induced by lindane in nematodes.