title: Bioactive peptide carnosin protects against lead acetate-induced hepatotoxicity by abrogation of oxidative stress in rats.
abstract: Context Oxidative stress is a common mechanism of liver injury. Carnosine is a dipeptide having strong antioxidant effects. Objectives We investigated the effects of carnosine on lead-induced hepatotoxicity and oxidative stress in rats. Materials and methods Animals received an aqueous solution of lead acetate (500 mg Pb/L in the drinking water) and/or daily oral gavage of carnosine (10 mg/kg) for 8 weeks. Rats were then weighed and used for the biochemical (commercial kits), molecular (standard chemical methods) and histological (microscopic) evaluations. Results Lead-induced oxidative stress in liver tissue was indicated by a significant increase in the level of malondialdehyde (MDA) (8.25 ± 0.15 nmol/mg) as well as decrease in the level of total antioxidant capacity (TAC) (1.72 ± 0.25 μmol/g) and total thiol (SH) groups) 1.9 ± 0.22 μmol/g). Carnosine treatment decreased MDA (4 ± 0.08 nmol/mg), whereas it increased the contents of total thiol (3.25 ± 0.04 μmol/g) and TAC (3.44 ± 0.32 μmol/g) in the lead group. Carnosine also prevented the decreased body weight (p < 0.001), albumin (p < 0.05) and total protein levels (p < 0.001) and increased liver weight (p < 0.05) and activates of hepatic enzymes (p's < 0.001) (alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase) in the lead group. Furthermore, histopathological study showed that carnosine attenuates liver damage by decreasing necrosis and infiltration of inflammatory cells. Conclusion Carnosine prevented lead-induced hepatotoxicity, indicated by molecular, biochemical and histopathological analyses through inhibiting lipid peroxidation and enhancing antioxidant defence systems. Therefore, carnosine makes a good candidate to protect against the deleterious effect of chronic lead intoxication.
authors.affiliation: a Department of Biology, School of Basic Sciences , Bu-Ali Sina University , Hamedan , Iran ;
authors.forename: Parisa
authors.initials: P
authors.lastname: Hasanein
authors.affiliation: a Department of Biology, School of Basic Sciences , Bu-Ali Sina University , Hamedan , Iran ;
authors.forename: Azam
authors.initials: A
authors.lastname: Kazemian-Mahtaj
authors.affiliation: b Department of Biochemistry, School of Medicine , Hamedan University of Medical Sciences , Hamedan , Iran.
authors.forename: Iraj
authors.initials: I
authors.lastname: Khodadadi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002336:Carnosine / Q000494:pharmacology*; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D019610:Cytoprotection; D004195:Disease Models, Animal; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D009929:Organ Size / Q000187:drug effects; D009942:Organometallic Compounds; D018384:Oxidative Stress / Q000187:drug effects*; D017208:Rats, Wistar
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D009942:Organometallic Compounds; D002336:Carnosine; C008261:lead acetate
keywords: Antioxidant; hepatoprotective; lipid peroxidation; liver; toxicity