Carnosine and taurine treatments diminished brain oxidative stress and apoptosis in D-galactose aging model

• Published in: Metabolic brain disease Vol. 31; no. 2; pp. 337 - 345
• Main Authors: Aydın, A. Fatih, Çoban, Jale, Doğan-Ekici, Işın, Betül-Kalaz, Esra, Doğru-Abbasoğlu, Semra, Uysal, Müjdat
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-04-2016; Springer Nature B.V
• Subjects: Aging; Animals; Antioxidants - pharmacology; Apoptosis - drug effects; Biochemistry; Biomedical and Life Sciences; Biomedicine; Carnosine - pharmacology; Galactose - metabolism; Glutathione Peroxidase - metabolism; Histidine - metabolism; Male; Malondialdehyde - metabolism; Metabolic Diseases; Neurology; Neurosciences; Oncology; Original Article; Oxidative Stress - drug effects; Rats, Wistar; Superoxide Dismutase - metabolism; Taurine - metabolism; Taurine - pharmacology; Taurine; Oxidative stress; Brain; Carnosine; D-Galactose
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-015-9755-0

D-galactose (GAL) has been used as an animal model for brain aging and antiaging studies. GAL stimulates oxidative stress in several tissues including brain. Carnosine (CAR; β-alanil-L-histidine) and taurine (TAU; 2-aminoethanesulfonic acid) exhibit antioxidant properties. CAR and TAU have anti-aging and neuroprotective effects. We investigated the effect of CAR and TAU supplementations on oxidative stress and brain damage in GAL-treated rats. Rats received GAL (300 mg/kg; s.c.; 5 days per week) alone or together with CAR (250 mg/kg/daily; i.p.; 5 days per week) or TAU (2.5 %
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; in rat chow) for 2 months. Brain malondialdehyde (MDA), protein carbonyl (PC) and glutathione (GSH) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), glutathione transferase (GST) and acetylcholinesterase (AChE) activities were determined. Expressions of B cell lymphoma-2 (Bcl-2), Bax and caspase-3 were also evaluated in the brains by immunohistochemistry. GAL treatment increased brain MDA and PC levels and AChE activities. It decreased significantly brain GSH levels, SOD and GSH-Px but not GST activities. GAL treatment caused histopathological changes and increased apoptosis. CAR and TAU significantly reduced brain AChE activities, MDA and PC levels and elevated GSH levels in GAL-treated rats. CAR, but not TAU, significantly increased low activities of SOD and GSH-Px. Both CAR and TAU diminished apoptosis and ameliorated histopathological findings in the brain of GAL-treated rats. Our results indicate that CAR and TAU may be effective to prevent the development of oxidative stress, apoptosis and histopathological deterioration in the brain of GAL-treated rats.