Cakatay Ufuk, Aydın Seval, Atukeren Pınar, Yanar Karolin, Sitar Mustafa E, Dalo Enis, Uslu Ezel
Department of Biochemistry, Istanbul University, Fatih, Istanbul, Turkey.
Curr Aging Sci. 2013 Jul;6(2):135-41. doi: 10.2174/18746098112059990034.
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.
氧化蛋白损伤增加和自由基介导的脱唾液酸化的氧化还原基础在衰老过程中尚未完全阐明。众所周知，几种肝脏疾病的发病率会随着年龄增长而增加。这项原创研究聚焦于拟衰老大鼠肝脏组织中的蛋白质氧化机制和蛋白结合唾液酸水平。对雄性Sprague-Dawley大鼠（20周龄）注射D-半乳糖（60毫克/千克/天），持续六周，以建立拟衰老模型。我们研究了各种蛋白质氧化标志物的组织水平，如蛋白质羰基、适宜的晚期氧化蛋白产物和蛋白质巯基。我们的研究还涉及了D-半乳糖诱导衰老大鼠肝脏组织中的蛋白结合唾液酸。与年轻对照组相比，衰老大鼠的蛋白质羰基（PCO）、蛋白质氢过氧化物（P-OOH）和晚期氧化蛋白产物（AOPP）水平显著更高。另一方面，两组之间未发现蛋白质巯基（P-SH）水平存在差异。与对照组相比，D-半乳糖诱导衰老大鼠的唾液酸（SA）水平显著更低。我们的结果表明，D-半乳糖诱导衰老大鼠对肝脏氧化蛋白损伤和肝细胞蛋白脱唾液酸化更敏感。这些分子机制可能在许多与年龄相关的肝脏疾病中起作用，这些疾病与氧化应激增加和氧化还原稳态改变有关。
