A redox basis of the increased oxidative protein damage and free radical-mediated desialylation have not been
fully elucidated in aging. It is well known that the incidence of several liver diseases increase with age. This original research
focuses on protein oxidation mechanisms and protein-bound sialic acid levels in liver tissue of the mimetic aging
rats. Injection of D-galactose (60 mg/kg/day) for six weeks to male Sprague-Dawley rats (20-week-old) used to establish
mimetic aging model. We investigated the tissue levels of various protein oxidation markers such as protein carbonyl
groups, suitable advanced oxidation protein products and protein thiol groups. Our study also covered protein-bound sialic
acid in liver tissue of D-galactose-induced aging rats. PCO (Protein Carbonyl Groups), P-OOH (Protein Hydroperoxides)
and AOPP (Advanced Oxidation Protein Products) levels in aging rats were significantly higher compared to young control
groups. On the other hand, P-SH (Protein Thiol Groups) levels were not found to be different between two groups. SA
(Sialic Acid) levels in D-galactose-induced aging rats were significantly lower compared to control groups. Our results
demonstrated greater susceptibility to hepatic oxidative protein damage and desialylation of hepatocellular proteins in Dgalactose-
induced aging rats. These molecular mechanisms may be operative in the many age-related liver diseases, which
are pertinent to increased oxidative stress and altered redox homeostasis.
Keywords: Aging, D-galactose, free radicals, protein oxidation, sialic acid.
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