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The effect of emodin on cytotoxicity, apoptosis and antioxidant capacity in the hepatic cells of grass carp (Ctenopharyngodon idellus).
- Source :
-
Fish & shellfish immunology [Fish Shellfish Immunol] 2014 May; Vol. 38 (1), pp. 74-9. Date of Electronic Publication: 2014 Mar 12. - Publication Year :
- 2014
-
Abstract
- 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.<br /> (Copyright © 2014 Elsevier Ltd. All rights reserved.)
Details
- Language :
- English
- ISSN :
- 1095-9947
- Volume :
- 38
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Fish & shellfish immunology
- Publication Type :
- Academic Journal
- Accession number :
- 24631735
- Full Text :
- https://doi.org/10.1016/j.fsi.2014.02.018