Abstract: Lindane, as one of persistent organic pollutants (POPs), has high toxicity, lipophilicity, chemical stability, and bioaccumulation. The use of lindane seriously threatens ecological environment and biosafety in China. Lindane bioaccumulation can cause liver function damage, but its toxic effects on liver have not been fully understood. In this study, we have investigated effects of lindane-induced oxidative stress on inflammation and autophagy in HepG2 cells. HepG2 cells were exposed to lindane for 24 h. Cell viability, intracellular reactive oxygen species (ROS), and autophagy were determined by thiazolyl blue (MTT) assay, 2,7-dichlorofluorescein (DCF) and immunofluorescence, respectively. The expression levels of IL-6, IL-8, IL-1β, TNF-α, NF-κB, Beclin1, ULK1 mRNA and P-P65, IL-1β, P62, LC3 protein were detected by real-time quantitative PCR and Western blot, respectively. We found that high-concentration lindane significantly decreased the cell viability, triggered an increase in both intracellular ROS and lactate dehydrogenase (LDH) levels, and decreased the catalase (CAT) activity. Moreover, the expression levels of TNF-α, IL-6, IL-1β, IL-8, NF-κB mRNA and P-p65, IL-1β, P62, LC3, and NF-κB protein were significantly up-regulated after lindane exposure. These results indicated that the lindane exposure causes oxidative stress and autophagy as well as inflammatory through activating NF-κB signaling pathway in HepG2 cells.

Key words: lindane, HepG2 cell, oxidative stress, inflammation, autophagy