Cadmium is a well-known environmental toxicant. At the cellular level, exposure to cadmium results in cytotoxic effects through the elevation of reactive oxygen species (ROS) production. Although cadmium exposure leads to the dysfunction of various organs, the underlying mechanisms of the toxic effects of cadmium in vivo are still largely unknown. Caenorhabditis elegans (C. elegans) is a useful model animal and exhibits unique biological reactions in response to environmental toxicants. In this study, the toxic mechanisms of cadmium exposure in C. elegans were investigated using N-acetylcysteine (NAC), which has dual functions, i.e., as a chelator of metals and as an antioxidant. NAC did not inhibit the uptake of cadmium into nematodes, suggesting that NAC did not function as a chelator of cadmium under these experimental conditions. Based on this finding, we investigated the effect of NAC as an antioxidant on representative phenotypic traits caused by cadmium exposure—reduced body length, aversion behavior, and shortened lifespan. NAC did not reverse the decreased body size but did clearly restore the aversion behavior and the shortened lifespan. These data suggest that aversion behavior and shortened lifespan are mediated by oxidative stress in C. elegans.

镉是一种众所周知的环境毒物。在细胞水平上，接触镉会通过增加活性氧 (ROS) 的产生而产生细胞毒性作用。尽管镉暴露会导致各种器官功能障碍，但镉在体内的毒性作用的潜在机制仍然很大程度上未知。Caenorhabditis elegans ( C. elegans ) 是一种有用的模型动物，在对环境毒物的反应中表现出独特的生物反应。在这项研究中，使用N研究了秀丽隐杆线虫中镉暴露的毒性机制-乙酰半胱氨酸(NAC)，具有双重功能，即作为金属螯合剂和作为抗氧化剂。NAC 不抑制镉被线虫吸收，这表明在这些实验条件下，NAC 不能起到镉螯合剂的作用。基于这一发现，我们研究了 NAC 作为抗氧化剂对镉暴露引起的代表性表型特征的影响——减少体长、厌恶行为和缩短寿命。NAC 并没有扭转体型的缩小，但确实恢复了厌恶行为和缩短的寿命。这些数据表明，厌恶行为和缩短的寿命是由秀丽隐杆线虫中的氧化应激介导的。