Prophylactic role of B vitamins against bulk and zinc oxide nanoparticles toxicity induced oxidative DNA damage and apoptosis in rat livers

ABSTRACT

The aim of this work is to explore the protective of B vitamins [B[3], B[6] and B[12]] against the hepatotoxic potency of either bulk zinc oxide [ZnO-bulk] or its nanoparticles [ZnO-NPs]-induced liver damage in rats. ZnO- bulk or its NPs were administered orally [500 mg/kg b.w.] for 10 successive days. The results revealed that oral coadministration of combination of B vitamins [250 mg B[3], 60 mg B[6] and 0.6 mg B[12] /Kg body weight] daily for 3 weeks to rats intoxicated by either ZnO- bulk or its NPs markedly ameliorated increases in serum of alanine aminotransferase [ALT], aspartate aminotransferase [AST] and lactate dehdrogenase [LDH]. The B vitamins also down-regulated increases in serum glucose level as well as increases in immuno-inflammatory biomarkers, including tumor necrosis factor- alpha [TNF- alpha] and C-reactive protein compared with intoxicated, untreated rats. Beside, the used agent successfully modulated the alterations in serum vascular endothelial growth factor [VEGF], attenuated liver oxidative DNA damage compared with ZnO intoxicated groups. We showed that the used B complex mitigated increased malondialdehyde [MDA], decrease in glutathione peroxidase [GPx] and increase in the apoptosis marker caspase 3 of liver tissue in response to either ZnO-bulk or its NP toxicity. In conclusion, early treatment with vitamin B complex may protect liver tissue from deleterious damage induced by the toxic effects of ZnO- bulk or its NPs