Effects of tefluthrin exposure on early life stages in zebrafish: Insights into cardiac and skeletal development, oxidative stress and apoptosis

Tefluthrin, a pyrethroid insecticide commonly used in soil, has raised concerns due to its widespread use and residual presence in aquatic environments. Nevertheless, studies on the toxicological mechanisms of tefluthrin at relevant concentrations during the early life stages of aquatic species remain limited. In this study, we assessed the developmental effects of tefluthrin exposure at concentrations of 1, 10, and 100 μg/L over 8 days on zebrafish embryos/larvae. Exposure to 100 μg/L of tefluthrin significantly reduced hatchability and survival rates, leading to cardiac edema and skeletal deformities. Alizarin Red and Alcian Blue staining showed reduced skeletal mineralization and disrupted craniofacial morphology. Importantly, tefluthrin exposure resulted in the dysregulation of important genes involved in heart and skeletal development, including nppa , vmhc , sox9b , gata4 , runx2a , shha , sp7 , and bmp2b . Mechanistically, tefluthrin exposure increased reactive oxygen species (ROS), decreased antioxidant enzyme activities (SOD, CAT), and elevated malondialdehyde (MDA). Furthermore, exposure to tefluthrin caused significant cell apoptosis in larvae, accompanied by dysregulation in the transcriptional expression of apoptotic genes ( bcl2 , bax , p53 , and caspase-3 ). Treatment with the antioxidant astaxanthin alleviated tefluthrin-induced oxidative stress and provided protection against heart and skeletal toxicity. In conclusion, this study demonstrated that tefluthrin's developmental toxicity affected heart and skeletal development, with mechanisms involving changes in gene expression, oxidative stress, and apoptosis, providing valuable insights for assessing environmental and food contamination risks.