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The effect of emodin on cytotoxicity, apoptosis and antioxidant capacity in the hepatic cells of grass carp (Ctenopharyngodon idellus)
- Cui, Yan-ting, Liu, Bo, Xie, Jun, Xu, Pao, Habte-Tsion, H.-Michael, Zhang, Yuan-yuan
- Fish & shellfish immunology 2014 v.38 no.1 pp. 74-79
- Ctenopharyngodon idella, antioxidant activity, apoptosis, cultured cells, cytotoxicity, dose response, emodin, free radical scavengers, glutathione, lactate dehydrogenase, membrane potential, mitochondria, mitochondrial membrane, oxidation, oxidative stress, reactive oxygen species, superoxide dismutase
- 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 cell's 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.