PubMed · 2010 · 45 citations · 45 references
PharmacyPharmacologyToxicologyHepatotoxicologyNutritional ToxicologyPharmaceutical ToxicologyBiomarkers Of Liver InjuryHepatic ToxicityHepatotoxicity ManagementHepatotoxicity MechanismsLiver DiseaseOxidative Stress In HepatotoxicityGamma-glutamyl TransferaseGlutathione Peroxidase ActivityGlutathione Reductase SystemHepatotoxic Plant CompoundsHistopathological ToxicityHistopathology Of Liver DiseaseLiver Toxicity MechanismsOxidative Stress In Liver Injury
Liver injury was induced in female rats using tamoxifen (TAM). Grape seeds (Vitis vinifera) extract (GSE), black seed (Nigella sativa) extract (NSE), curcumin (CUR) or silymarin (SYL) were orally administered to TAM-intoxicated rats. Liver histopathology of TAM-intoxicated:rats showed pathological changes. TAM-intoxication elicited declines in liver antioxidant enzymes levels (glutathione peroxidase, glutathione reductase, superoxide dismutase and catalase), reduced glutathione (GSH) and GSH/GSSG ratio plus the hepatic elevations in lipid peroxides, oxidized glutathione (GSSG), tumor necrosis factor-alpha (TNF-alpha) and serum liver enzymes; alanine transaminase, aspartate transaminase, alkaline phosphatase, lactate dehydrogenase and gamma glutamyl transferase levels. Oral intake of NSE, GSE, CUR or SYL to TAM-intoxicated rats, attenuated histopathological changes and corrected all parameters mentioned above. Improvements were prominent in case of NSE (similarly SYL) > CUR > GSE. Data indicated that NSE, GSE or CUR act as free radicals scavengers and protect TAM-induced liver injury in rats.
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