School of Life Science, Shanxi University, Taiyuan 030006, China.
Comp Biochem Physiol C Toxicol Pharmacol. 2012 Nov;156(3-4):195-201. doi: 10.1016/j.cbpc.2012.05.006. Epub 2012 Jun 9.
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 (H(2)O(2)) 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 H(2)O(2) after 2 h of treatment at 58 mg L(-1) Cd, and significantly increased the caspase-3/8/9 activity in crabs relative to the control group. Pre-treatment with the scavenger for H(2)O(2), 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 H(2)O(2) generation to trigger the crab apoptotic processes by regulating the activities of caspase enzymes.
镉(Cd)是一种众所周知的有毒重金属,会在水生环境中积累。已有报道称,镉会诱导氧化损伤和细胞凋亡。我们研究了过氧化氢(H₂O₂)对镉诱导细胞凋亡的调控机制。我们发现,在淡水蟹河南华溪蟹的鳃组织中,镉以时间和浓度依赖的方式诱导细胞凋亡,这一结论通过 DNA 片段化分析和透射电子显微镜得到了证实。此外,在 58 mg L(-1) Cd 处理 2 小时后,镉会导致 H₂O₂的产生,并且与对照组相比,镉会显著增加蟹体内 caspase-3/8/9 的活性。用 H₂O₂清除剂二甲基硫脲(DMTU)和抗氧化剂 N-乙酰半胱氨酸(NAC)预处理可以有效抑制 caspase-3 和 caspase-9 的活性,最终阻止了镉诱导的 DNA 片段化和凋亡细胞死亡的标志物的出现。这些结果表明,镉可能通过调节半胱天冬酶酶的活性来诱导细胞内 H₂O₂的产生,从而触发蟹的凋亡过程。