α-tocopherol ameliorates copper II oxide nanoparticles-induced cytotoxic, biochemical, apoptotic, and genotoxic damages in the rainbow trout gonad cells-2 (RTG-2) culture

We investigated the effects of α-tocopherol on oxidative stress-caused damage caused by copper II oxide nanoparticles (CuO NPs) on Oncorhynchus mykiss gonadal cells (RTG-2) for 24 and 48 h. α-Tocopherol reversed the cell death and alterations in the expressions of genes such as sod1, gpx1a, gpx4b, and igf2 caused by CuO NPs; it also supported the expressions of cat, igf1, and gapdh genes caused by CuO NPs for 24 h and promoted alterations in the expressions of the sod2, gh1, and igf1 genes for 48 h. Additionally, α-tocopherol reversed the caspase 3/7 activity increased by CuO NPs for 24 h and supported it’s decrease for 48 h. α-Tocopherol supported the increase in tail DNA (%) affected by CuO NPs for 24 h and reversed it for 48 h. Therefore, α-tocopherol may have the potential to protect against cellular alterations induced by CuO NPs in a time-dependent manner. •CuO NPs caused cytotoxicity, caspase 3/7 activity and tail DNA in the RTG-2 cells.•Tocopherol reduced cytotoxicity, caspase 3/7 activity induced by CuO NPs.•Tocopherol did not make a significant impact on antioxidant enzyme genes at 48 h.•Tocopherol supported the expressions of growth genes (gh1, igf1) changed by CuO NPs.•Tocopherol decreased the expression of the glycolytic gene compared to CuO NPs.