Immunotoxicology Lab, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow, India.
Toxicology. 2011 Sep 5;287(1-3):46-53. doi: 10.1016/j.tox.2011.05.013. Epub 2011 May 30.
Cadmium is a common environmental and occupational hazard and its adverse effect on reproductive organ has been well documented. The present study is planned to delineate the mechanism of Cd toxicity in rat testes. Our study shows that Cd causes apoptosis in sertoli-germ cells which is governed by oxidative stress. We assayed ROS, GSH and MMP to ensure the role of oxidative stress, further confirmed it by thiol modulators. The initial biochemical response shown in sertoli-germ cells was a significant rise in intracellular calcium followed by a drastic fall in MMP and then ROS generation. The downstream events included cytochrome c release leading to caspase-3 activation and culminating in cell death via apoptosis. Furthermore Cd disrupted the spermatogenic pathway as evident by suppression in tesmin and LDH-X levels.
镉是一种常见的环境和职业危害物，其对生殖器官的不良影响已有充分的文献记载。本研究旨在阐述镉对大鼠睾丸毒性的作用机制。我们的研究表明，镉通过氧化应激导致支持细胞-生殖细胞凋亡。我们检测了 ROS、GSH 和 MMP 以确定氧化应激的作用，并通过巯基调节剂进一步证实了这一点。支持细胞-生殖细胞的初始生化反应是细胞内钙显著升高，随后 MMP 急剧下降，然后 ROS 生成。下游事件包括细胞色素 c 释放导致 caspase-3 激活，最终通过细胞凋亡导致细胞死亡。此外，镉还破坏了精子发生途径，表现为 tesmin 和 LDH-X 水平的抑制。
