Chlorantraniliprole-induced oxidative stress, DNA damage, and apoptosis in Caenorhabditis elegans: Mechanistic insights and ecological risk implications

Chlorantraniliprole (CAP) is one of the most widely used insecticides in the world. CAP is strictly restricted in foodstuff with maximum residual limits (MRLs) from 0.01 to 40 mg/kg set by Chinese national food safety standard. However, a detailed evaluation on its possible acute toxicity and the underlying mechanisms remains inconclusive. In this study, effects of CAP at environmentally relevant concentrations on growth, locomotion, lifespan, reproduction, and antioxidative defense systems were evaluated using the model organism Caenorhabditis elegans. Exposure to CAP notably reduced nematode development, head thrash, and pharyngeal pumping frequency compared with the control. Moreover, CAP at 0.1, 1, and 10 μg/L decreased lifespan of nematodes by 23.73 %, 28.71 %, and 36.23 %, respectively. CAP at 1 and 10 μg/L enhanced the ROS level, reduced the activity of antioxidative enzyme, including CAT and SOD. CAP also regulated mRNA expression levels of daf-16, skn-1, sod-3, gst-4, ced-3, ced-4, ced-9, egl-1, clk-2, and hus-1 in the nematodes, while no significant effect in the mutants was observed. Pearson correlation analysis revealed that significant correlation existed between tested parameters, indicating that CAP caused a series of negative effects in the nematodes. Meanwhile, molecular docking results revealed the potential of CAP to bind with oxidative stress, DNA damage and apoptosis proteins, providing molecular mechanisms for the observed detrimental effects. Therefore, our results suggested that acute exposure to CAP at environmental concentrations caused oxidative stress, DNA damage and apoptosis in the nematodes. Our results shed new light on risk assessment and management of CAP.