2012 · 12 citations · 8 references
Veterinary MedicinePharmacologyToxicologyDevelopmental ToxicologyHeavy Metal ToxicologyHepatotoxicologyArsenic ToxicologyHepatotoxicity MechanismsOxidative Stress In HepatotoxicityPrenatal ToxicityArsenic-induced Liver ToxicityGlutathione Peroxidase ActivityGlutathione S-transferasesHepatoprotective AgentsHistopathological ToxicityLipid Peroxidation In HepatotoxicityLipid Peroxidation MarkersOxidative Stress Injury
2 Abstract: Oxidative stress was induced by oral administration 0.4 mg/kg b.wt of arsenic trioxide (As O ,) during 23 embryonic development in experimental mice. The level of liver arsenic concentration, lipid peroxidation, reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione-S-transferase (GST) and glutathione peroxidase (GPx) were determined in adult male Swiss Albino Mice. Hepatotoxicity was assessed by quantifying the aspartate transaminase (AST), alanine transaminase (ALT) and alkaline phophatase (ALP). Hepatoprotective efficacy of curcumin (7.5mg/kg b.wt) was evaluated by combination treatment with As O The theme of our study was to evaluate the efficacy of curcumin in 2 3. combating arsenic induced hepatic oxidative stress, histopathological changes and the hepatic arsenic accumulation in mice model. Results revealed that As2O3 administration leads to the generation of reactive oxygen species (ROS), arsenic accumulation, serum marker enzymes release and decrease in antioxidant enzymes in liver. Retention of arsenic in liver caused increased level of lipid peroxidation with a concomitant decline in the glutathione dependant antioxidant enzymes and antiperoxidative enzymes. Curcumin treatment protected the liver from arsenic induced deterioration of antioxidant levels as well as oxidative stress. And also a significant decrease in hepatic arsenic accumulation and serum marker enzymes was observed. Histopathological examination revealed a protective effect of curcumin to liver tissue. From arsenic-induced toxic effects during embryonic development.
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