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. [ABSTRACT FROM AUTHOR]