Toxic effects of benzovindiflupyr, a new SDHI-type fungicide on earthworms (Eisenia fetida)

Benzovindiflupyr has received increasing attention as a new novel succinate dehydrogenase inhibitor (SDHI)-type fungicide. Nonetheless, its traces remaining in soil potentially trigger an ecotoxicological threat to soil organisms including earthworms. This paper evaluates the eco-toxicity of different benzovindiflupyr doses (0.1, 1, 5, and 10 mg kg(-1)) on earthworms (Eisenia fetida) after long-term exposure. Consequently, benzovindiflupyr at higher doses significantly inhibited the activities of respiratory chain complex II and succinate dehydrogenase (SDH) in E. fetida. Besides, the reactive oxygen species (ROS) and lipid peroxidation (LPO) were significantly induced in earthworms when treated with this fungicide. After benzovindiflupyr exposure, activities of antioxidant enzymes including catalase, peroxidase, and superoxide dismutase were activated. However, glutathione S-transferase activity in E. fetida was initially induced then inhibited in earthworms after treatment. Furthermore, benzovindiflupyr exposure induced the protein carbonylation (PCO) level in cells indicating oxidative damage to the cellular protein. Due to the destruction of the normal function in the coelomocytes, the phagocytic activity was initially activated, then inhibited when earthworms were treated at 5 and 10 mg kg(-1) concentrations. Additionally, DNA damage was induced (larger olive tail moment (OTM) values) with the increase of benzovindiflupyr doses and exposure time. The weight was significantly decreased after benzovindiflupyr exposure on days 21 and 28. Benzovindiflupyr at higher doses significantly decreased the reproduction (number of cocoons and juveniles) of E. fetida. These findings reveal that benzovindiflupyr potentially induces a potential toxicological risk to earthworms when applied in the mentioned above dosages.

Automated summary

Benzovindiflupyr poses a potential toxicological risk to earthworms by inhibiting respiratory chain and SDH, inducing antioxidant enzymes, LPO, and PCO, leading to DNA damage and decreased reproductive ability.