Abstract: The freshwater, bloom-forming cyanobacterium (blue-green alga) Microcystis aeruginosa produces a peptide hepatotoxin (microcystins, MC), which causes the damage of animal liver. Recently, toxic Microcystis blooms frequently occur in the eutrophic lake and have caused many troubles to the environment in China. Microcystins remained in water supply also become the severe threat to people health. Microcystin-LR from Microcystiswas isolated and purified with high performance liquid chromatography (HPLC) and its toxicity to mouse and fish liver were partly studied (Li et al., 2001). In this study, six indexes (Reactive oxygen species, Glutathione, Superoxide dismutase, Catalase, Glutathione peroxide and Glutathione S-transferase) in common carp hepatocytes were determined with the kits supplied by the Nanjing Bioengineering Institute when the cells were exposed to 10μg/L microcystin-LR. The results showed that Reactive oxygen species (ROS) contents increased obviously after 6h exposure to the toxin. In contrast, Glutathione (GSH) levels in the hepatocytes exposed to microcystin-LR decreased by 47% compared with the control. The activities of Superoxide dismutase (SOD), Catalase (CAT) and Glutathione peroxide (GSH-Px) increased after 6h exposure to microcystin-LR, but Glutathione S-transferase (GST) activity showed no difference with the control. These results suggested that the toxicity of microcystin-LR caused the increase of ROS contents and the depletion of GSH in hepatocytes exposed to the toxin and these changes led to oxidant shock in hepatocytes. Activities increases of SOD, CAT and GSH-Px revealed that these three kinds of antioxidant enzymes might play important roles in eliminating the excessive ROS. From the present study, we could infer the possible toxicity mechanism of microcystin-LR on the common carp hepatocytes. MC can potently inhibit protein phosphatase type-1 and 2A after the toxin were transported to cytoplasm by the bile acid transporter in the cell membrane of hepatocytes and the inhibition may disturb the cellular phosphorylation balance, cause the marked increase of ROS contents and the depletion of GSH in hepatocytes. As a result, these changes would lead to oxidant shock in the hepatocytes. Although antioxidant enzymes (SOD, CAT and GSH-Px) had played their roles in eliminating cytosolic ROS and regenerating GSH, they could not prevail over the oxidant stress induced by the toxin. Therefore, these effects caused the damages of hepatocytes, leading to apoptosis and even necrosis of cells.