Influences of l-ascorbic acid on cytotoxic, biochemical, and genotoxic damages caused by copper II oxide nanoparticles in the rainbow trout gonad cells-2.

In parallel with the raising use of copper oxide nanoparticles (CuO NPs) in various industrial and commercial practices, scientific reports on their release to the environment and toxicity are increasing. The toxicity of CuO NPs is mostly based on their oxidative stress. Therefore, it is necessary to investigate the efficacy of well-known therapeutic agents as antioxidants against CuO NPs damage. This study aimed to investigate the mechanism of this damage and to display whether l-ascorbic acid could preserve against the cell toxicities induced by CuO NPs in the rainbow trout gonad cells-2 (RTG-2). While CuO NPs treatment significantly diminished cell viability, the l-ascorbic acid supplement reversed this. l-ascorbic acid treatment reversed the changes in expressions of sod1, sod2, gpx1a, and gpx4b genes while playing a supportive role in the changes in the expression of the cat gene induced by CuO NPs treatment. Moreover, CuO NPs treatment caused an upregulation in the expressions of growth-related genes (gh1, igf1, and igf2) and l-ascorbic acid treatment further increased these effects. CuO NPs treatment significantly up-regulated the expression of the gapdh gene (glycolytic enzyme gene) compared to the control group, and l-ascorbic acid treatment significantly down-regulated the expression of the gapdh gene compared to CuO NPs treatment. The genotoxicity test demonstrated that l-ascorbic acid treatment increased the genotoxic effect caused by CuO NPs by acting as a co-mutagen. Based on the findings, l-ascorbic acid has the potential to be sometimes inhibitory and sometimes supportive of cellular mechanisms caused by CuO NPs.