Fluopyram, a succinate dehydrogenase inhibitor fungicide and nematicide, has been used extensively for agricultural pest control and toxicologically affects non-target organisms. In the present study, Caenorhabditis elegans, a well-established model organism, was used to evaluate the toxic effect of fluopyram and the possible molecular mechanisms. C. elegans was exposed to fluopyram for 24 h at three sublethal concentrations (0.01, 0.05 and 0.25 mg/L) and the physiological, biochemical, and molecular indicators were examined. The results showed that sublethal exposure to fluopyram could cause damage to growth, locomotion behavior, feeding, lifespan and reproduction of the nematodes. Fluopyram exposure induced oxidative stress as indicated by increase of ROS production, lipofuscin and lipid accumulation, and MDA level in the nematodes. In contrast, exposure to fluopyram significantly decreased the activities of target enzyme SDH and antioxidant enzymes including SOD, CAT and GST. Moreover, the expression of genes associated with oxidative stress (e.g., gst-4, sod-3, fat-7, mev-1 and daf-16), intestinal damage (e.g., mtm-6, nhx-2, opt-2, pkc-3, par-6, act-5 and egl-8), and cell apoptosis (e.g., ced-13, ced-3, egl-38, efl-2, cep-1 and lgg-1) was significantly influenced after exposure to fluopyram. According to Pearson correlation analyses, significant correlation existed between 190 pairs of parameters, which indicated that fluopyram induced multiple toxic related effects in C. elegans. These findings suggest that oxidative stress, intestinal damage, and cell apoptosis may play major roles in toxicity of fluopyram in the nematodes.
Keywords: Caenorhabditis elegans; Cell apoptosis; Fluopyram; Intestinal damage; Oxidative stress; Toxic effect.
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