The effect of emodin on cytotoxicity, apoptosis and antioxidant capacity in the hepatic cells of grass carp (Ctenopharyngodon idellus)

We determined the effect of emodin on the lactate dehydrogenase (LDH) release, superoxide dismutase (SOD), glutathione (GSH), total antioxidant capacity (T-AOC), reactive oxygen species (ROS), mitochondria membrane potential (ΔΨm), and apoptosis in the hepatic cells of grass carp (Ctenopharyngodon idellus). Cultured cells were treated with different concentrations of emodin (0.04–25 μg/ml) for 24 h. We found that the cytotoxic effect of emodin was mediated by apoptosis, and that this apoptosis occurred in a dose-dependent manner. Emodin (1–25 μg/ml) significantly induced apoptosis accompanying by ΔΨm disruption and ROS generation and significantly reduced the SOD activities and T-AOC compared to the control. Thus, the oxidative effect of emodin may be attributed to the loss of the cellʹs ability to maintain the activity of its radical-scavenging enzymes. GSH was also significantly higher after 0.2–1 μg/ml emodin exposure, indicating that cells failed to maintain their redox balance when compensating for the increased oxidative stress. Our results suggest that emodin (1–25 μg/ml) exerts its cytotoxic effects via apoptosis by directly affecting the mitochondria.