Cadmium Toxicity in Caenorhabditis elegans: Mechanisms and Interventions by Vitamin C and Fruit Juices

With the rapid development of industry, heavy metal pollution has emerged as a significant threat to food safety and human health. Among these pollutions, cadmium (Cd) pollution has become a global environmental concern. Caenorhabditis elegans, with its short life cycle and evolutionary conservation with humans, serves as an ideal model organism for studying toxicity mechanisms. In this study, we investigated the mechanisms of toxicity induced by Cd in C. elegans and the intervention of ascorbic acid (VC) and fruit juices on toxicity induced by Cd. Using fluorescent probes, we observed that Cd exposure (5 mg/mL and 8 mg/mL of CdCl2) significantly decreased the vitality of C. elegans in a dose-dependent manner within 6 h. Reactive oxygen species (ROS) and nitric oxide (NO) accumulated concurrently. Further exploration revealed that ROS played a crucial role in Cd-induced acute toxicity. The inhibition of ROS by Imidazole (IMZ) and Pyridine (PY) not only reduced NO levels but also restored the vitality of C. elegans. Conversely, the removal of NO by cPTIO [2-(4-Carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide] or L-NMMA (NG-Monomethyl-L-arginine) improved the vitality; however, it still did not affect ROS levels, indicating that ROS accumulation is a primary event in Cd-induced toxicity. We also examined the protective effects of VC and fruit juices. Both VC (0.5 mg/mL, 1 mg/mL) and fruit juices (50% (v/v) of the total volume of the medium) significantly enhanced the vitality of C. elegans under CdCl2 stress and reduced the accumulation of ROS and NO. This suggests that VC-rich materials effectively scavenge ROS and NO, thereby alleviating Cd-induced oxidative stress and toxicity. In summary, our results elucidate that CdCl2 exposure leads to ROS accumulation in C. elegans, which in turn triggers NO production and ultimately reduces nematode activity. VC and VC-rich materials can effectively mitigate CdCl2 toxicity by scavenging ROS and NO, providing a potential strategy for alleviating Cd poisoning.