OBJECTIVES: Potential health hazard is associated with the wide use of nanoparticles. The prophylactic role of either α-lipoic acid (α-lip) or vitamin E (vit E) against the toxic effect of zinc oxide nano-particles (ZnO-NPs) induced metabolic disorder, inflammation and DNA damage in rat livers was studied. MATERIALS AND METHODS: ZnO-NPs were administered orally using two doses (600 mg and 1 g/kg body weight/day for 5 conscutive days). Some biomarkers of tissue damage, metabolic disorder, and DNA damage were investigated to explore the protective mechanisms of α-lip or vit E against ZnO-NPs induced hepatotoxicity. RESULTS: Co-administration of either α-lip (200 mg/kg body weight) or vit E (100 mg/kg body weight) daily for three weeks to ZnO-NPs intoxicated rats, significantly down-modulated the marked increase in serum ALT (marker of liver damage) and also serum glucose level (marker of metabolic disorder) as well as the pro-inflammatory biomarkers including nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), and immunoglobin G (IGg). Reduced glutathione level was decreased while caspase3 level was elevated in liver tissues of ZnO-NPs treated group compared with intoxicated one. Moreover histopathological examination of liver tissue supported the previous biochemical markers. Furthermore, ZnO-NPs induced hepatic oxidative DNA damage. CONCLUSIONS: Either α-lip or vit E proved to be hepatoprotective agents against ZnO-NPs toxicity because they ameliorated metabolic and immune disorders related to liver damage and modulated the previous measured parameters.
OBJECTIVES: Potential health hazard is associated with the wide use of nanoparticles. The prophylactic role of either α-lipoic acid (α-lip) or vitamin E (vit E) against the toxic effect of zinc oxide nano-particles (ZnO-NPs) induced metabolic disorder, inflammation and DNA damage in rat livers was studied. MATERIALS AND METHODS:ZnO-NPs were administered orally using two doses (600 mg and 1 g/kg body weight/day for 5 conscutive days). Some biomarkers of tissue damage, metabolic disorder, and DNA damage were investigated to explore the protective mechanisms of α-lip or vit E against ZnO-NPs induced hepatotoxicity. RESULTS: Co-administration of either α-lip (200 mg/kg body weight) or vit E (100 mg/kg body weight) daily for three weeks to ZnO-NPs intoxicated rats, significantly down-modulated the marked increase in serum ALT (marker of liver damage) and also serum glucose level (marker of metabolic disorder) as well as the pro-inflammatory biomarkers including nitric oxide (NO), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), C-reactive protein (CRP), and immunoglobin G (IGg). Reduced glutathione level was decreased while caspase3 level was elevated in liver tissues of ZnO-NPs treated group compared with intoxicated one. Moreover histopathological examination of liver tissue supported the previous biochemical markers. Furthermore, ZnO-NPs induced hepatic oxidative DNA damage. CONCLUSIONS: Either α-lip or vit E proved to be hepatoprotective agents against ZnO-NPs toxicity because they ameliorated metabolic and immune disorders related to liver damage and modulated the previous measured parameters.