Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8319219 | Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology | 2012 | 7 Pages |
Abstract
Cadmium (Cd) is a well-known toxic heavy metal that accumulates in the aquatic environment. Cd has been reported to induce oxidative damage and apoptosis. We investigated the regulation mechanism of hydrogen peroxide (H2O2) on Cd-induced apoptosis. We show that in the gills of the freshwater crab Sinopotamon henanense Cd induced apoptosis, in a time- and concentration-dependent manner, as confirmed by DNA fragmentation analysis and transmission electron microscopy. Additionally, Cd caused production of H2O2 after 2 h of treatment at 58 mg Lâ 1 Cd, and significantly increased the caspase-3/8/9 activity in crabs relative to the control group. Pre-treatment with the scavenger for H2O2, dimethylthiourea (DMTU) and antioxidant, N-acetyl cysteine (NAC), effectively inhibited the activities of caspase-3 and caspase-9, eventually blocked Cd-induced DNA fragmentation and the appearance of markers for apoptotic cell death. These results suggest that Cd might induce intracellular H2O2 generation to trigger the crab apoptotic processes by regulating the activities of caspase enzymes.
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Authors
Jinxiang Wang, Qian Wang, Jiarui Li, Qingqing Shen, Fei Wang, Lan Wang,