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

• Published in: Pakistan journal of pharmaceutical sciences Vol. 28; no. 1; pp. 175 - 184
• Main Authors: Yousef, Jehad Mustafa, Mohamed, Azza Mostafa
• Format: Journal Article
• Language: English
• Published: Pakistan 01.01.2015
• Subjects: Administration, Oral; Animals; Antioxidants - administration & dosage; Antioxidants - pharmacology; Apoptosis - drug effects; Biomarkers - blood; Chemical and Drug Induced Liver Injury - blood; Chemical and Drug Induced Liver Injury - etiology; Chemical and Drug Induced Liver Injury - pathology; Chemical and Drug Induced Liver Injury - prevention & control; Cytoprotection; DNA Damage; Inflammation Mediators - blood; Liver - drug effects; Liver - metabolism; Liver - pathology; Male; Metal Nanoparticles; Oxidative Stress - drug effects; Rats, Sprague-Dawley; Time Factors; Vitamin B Complex - administration & dosage; Vitamin B Complex - pharmacology; Zinc Oxide
• ISSN: 1011-601X

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 co-administration 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-α (TNF-α) 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.