Cebe Tamer, Atukeren Pınar, Yanar Karolin, Kuruç Aylin Irmak, Ozan Tuna, Kunbaz Ahmad, Sitar Mustafa Erinç, Mirmaroufizibandeh Reza, Aydın Seval, Çakatay Ufuk
Cerrahpaşa Faculty of Medicine, Istanbul University, Turkey.
Department of Medical Biochemistry, Cerrahpaşa Faculty of Medicine, Istanbul University, Turkey.
Exp Gerontol. 2014 Sep;57:132-40. doi: 10.1016/j.exger.2014.05.017. Epub 2014 May 28.
The effect of the natural aging process on systemic redox homeostasis is previously documented. However, none of the studies specify the effect of experimental aging on systemic redox homeostasis. The purpose of this study is to clarify the ambiguity raised in preliminary reports as to mimetic aging dependency of the type and magnitude of oxidative damage on constituents of plasma.
In the current study, we investigated the interrelationship among various groups of the systemic oxidative damage markers such as protein oxidation products (protein carbonyl groups, protein hydroperoxides, advanced oxidation protein products, protein thiol groups), lipid peroxidation products (malondialdehyde, lipid hydroperoxides, conjugated dienes), glycoxidation adducts (advanced glycation end products), and antioxidant capacity (ferric reducing/antioxidant power, Cu,Zn-superoxide dismutase, total thiol, non-protein thiol). All these markers were measured in plasma of mimetically aged (MA) rats (5-month-old rats subjected to d-galactose-induced experimental aging), naturally aged (NA) rats (24-month-old), and their corresponding young controls (YC) (5months old).
Our current results show that systemic oxidation markers of the MA group share significant similarities in terms of impaired redox homeostasis with the NA rats and may be considered as a reliable experimental aging model for intravascular aging. Additional methodological studies including d-galactose dosage and application time are warranted to clarify the potential involvement of all these systemic redox variations as mechanistic factors in the development of mimetic aging related intravascular deterioration. Reversing or preventing systemic oxidative damage in experimental and natural aging should therefore be considered the primary target for the development of effective therapeutic strategies to prevent or treat age-related vascular disorders.
自然衰老过程对全身氧化还原稳态的影响已有文献记载。然而，尚无研究明确实验性衰老对全身氧化还原稳态的影响。本研究的目的是澄清初步报告中提出的关于氧化损伤类型和程度对血浆成分的模拟衰老依赖性的模糊之处。
在本研究中，我们调查了全身氧化损伤标志物的不同组之间的相互关系，如蛋白质氧化产物（蛋白质羰基、蛋白质氢过氧化物、晚期氧化蛋白产物、蛋白质巯基）、脂质过氧化产物（丙二醛、脂质氢过氧化物、共轭二烯）、糖氧化加合物（晚期糖基化终产物）和抗氧化能力（铁还原/抗氧化能力、铜锌超氧化物歧化酶、总巯基、非蛋白质巯基）。所有这些标志物均在模拟衰老（MA）大鼠（5月龄大鼠接受d-半乳糖诱导的实验性衰老）、自然衰老（NA）大鼠（24月龄）及其相应的年轻对照（YC）（5月龄）的血浆中进行测量。
我们目前的结果表明，MA组的全身氧化标志物在氧化还原稳态受损方面与NA大鼠具有显著相似性，可被视为血管内衰老的可靠实验性衰老模型。有必要进行包括d-半乳糖剂量和应用时间在内的额外方法学研究，以阐明所有这些全身氧化还原变化作为模拟衰老相关血管内恶化发展的机制因素的潜在参与情况。因此，逆转或预防实验性和自然衰老中的全身氧化损伤应被视为制定有效治疗策略以预防或治疗与年龄相关的血管疾病的主要目标。
