title: Carnosine and taurine treatments decreased oxidative stress and tissue damage induced by D-galactose in rat liver.
abstract: D-galactose (GAL) causes aging-related changes and oxidative stress in the organism. We investigated the effect of carnosine (CAR) or taurine (TAU), having antioxidant effects, on hepatic injury and oxidative stress in GAL-treated rats. Rats received GAL (300 mg/kg; s.c.; 5 days/week) alone or together with CAR (250 mg/kg/daily; i.p.; 5 days/week) or TAU (2.5 % w/w; in rat chow) for 2 months. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and hepatic malondialdehyde (MDA), protein carbonyl (PC) and glutathione (GSH) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-0050x), and glutathione transferase (GST) activities were determined. Hepatic expressions of B cell lymphoma-2 (Bcl-2), Bax and Ki-67 were evaluated. Serum ALT, AST, hepatic MDA, and PC levels were observed to increase in GAL-treated rats. Hepatic Bax expression, but not Bcl-2, increased, Ki-67 expression decreased. GAL treatment caused decreases in GSH levels, SOD and GSH-Px activities in the liver. Hepatic mRNA expressions of SOD, but not GSH-Px, also diminished. CAR or TAU treatments caused significant decreases in serum ALT and AST activities. These treatments decreased apoptosis and increased proliferation and ameliorated histopathological findings in the livers of GAL-treated rats. Both CAR and TAU reduced MDA and PC levels and elevated GSH levels, SOD and GSH-Px (non significant in TAU + GAL group) activities. These treatments did not alter hepatic mRNA expressions of SOD and GSH-Px enzymes. Our results indicate that CAR and TAU restored liver prooxidant status together with histopathological amelioration in GAL-induced liver damage.
authors.affiliation: Department of Biochemistry, Istanbul Medical Faculty, Istanbul University, Çapa, Istanbul, Turkey.
authors.forename: Esra Betül
authors.initials: EB
authors.lastname: Kalaz
authors.forename: Jale
authors.initials: J
authors.lastname: Çoban
authors.forename: A Fatih
authors.initials: AF
authors.lastname: Aydın
authors.forename: Işın
authors.initials: I
authors.lastname: Doğan-Ekici
authors.forename: Semra
authors.initials: S
authors.lastname: Doğru-Abbasoğlu
authors.forename: Serdar
authors.initials: S
authors.lastname: Öztezcan
authors.forename: Müjdat
authors.initials: M
authors.lastname: Uysal
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001219:Aspartate Aminotransferases / Q000097:blood; D002336:Carnosine / Q000494:pharmacology*; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy* / Q000378:metabolism; D005690:Galactose / Q000633:toxicity*; D008099:Liver / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D050050:Protein Carbonylation; D051381:Rats; D017208:Rats, Wistar; D013654:Taurine / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D013654:Taurine; D008315:Malondialdehyde; D002336:Carnosine; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D005690:Galactose