Time‑order effects of vitamin C on hexavalent chromium‑induced mitochondrial damage and DNA‑protein crosslinks in cultured rat peripheral blood lymphocytes.

摘要: Hexavalent chromium [Cr(VI)] and its compounds have extensive applications in many industries are widely known to cause occupational diseases as well carcinogenic effects humans. Mitochondrial damage, which is important Cr(VI)‑induced cytotoxicity, may be characterized by the opening status of permeability transition pore, maintenance mitochondrial membrane potential level malondialdehyde. The formation DNA‑protein crosslinks (DPCs) target tissues appears direct primary genotoxic effect Cr(VI) exposure, lymphocytic DPCs viewed a biomarker internal accumulation. It that vitamin C (vit C) an biological reducing agent humans animals, capable Cr(VI). Regardless evidence from cell culture in vivo experiments protective antioxidant, vit C, following exposure Cr(VI), no studies been conducted date demonstrate time‑order vit C on damage DPC formation. In present study, using peripheral blood lymphocytes Sprague‑Dawley rats, we demonstrated pre‑ co‑treatment against loss viability while only has increase DPCs. mechanistic investigation revealed cellular reactive oxygen species levels correlated with p53 expression We concluded exerts different formation, biomarkers, including p53, used assessment development cancer. These findings facilitate more detailed follow‑up Cr(VI)‑exposure populations for secondary prevention.