Akademik Veri Yönetim Sistemi
Rejuvenation research, cilt.18, sa.4, ss.299-312, 2015 (SCI-Expanded)
Background: Testosterone biosynthesis gradually decreases with age. Impaired redox homeostasis-related oxidative damage in cellular macromolecules has a high risk for the development of renal insufficiency. Our aim was to study the effects of testosterone replacement therapy on redox homeostasis. Methods: We investigated various oxidative damage biomarkers in kidney. Experimental animals were separated into three groupsnaturally aged rats, testosterone-administered naturally aged rats (single dose of 25mg/kg testosterone enanthate), and their respective young controls. Results: Our results showed that the testosterone-administered naturally aged group shared significant similarities with the young rats with respect to their redox status. In testosterone-administered naturally aged rats, kynurenine, protein carbonyl, advanced oxidation protein products, lipid peroxidation markers, and xanthine oxidase activities were significantly lower and Cu-Zn superoxide dismutase activities and testosterone levels were higher than naturally aged rats. In testosterone-administered naturally aged rats, catalase activities, ferric reducing anti-oxidant power, and testosterone levels were significantly lower and dityrosine, N-formyl kynurenine, protein carbonyl, and protein hydroperoxides were significantly higher than in young rats. On the other hand, in naturally aged rats, Cu-Zn superoxide dismutase, catalase activities, ferric reducing anti-oxidant power, and testosterone levels were lower and dityrosine, kynurenine, protein carbonyl, protein hydroperoxide, advanced oxidation protein products, lipid peroxidation markers, advanced glycation end products, and xanthine oxidase activities were higher than controls. Conclusions: Our results showed that a single dose of testosterone administration has a positive effect on the redox status of the aged kidney. Future studies are needed to clarify the exact molecular mechanism(s) involved in the action of testosterone in maintaining kidney redox homeostasis.