QOPNA, Chemistry Department, University of Aveiro, Campus de Santiago, 3810-193 Aveiro, Portugal.
Eur J Appl Physiol. 2012 Apr;112(4):1467-74. doi: 10.1007/s00421-011-2100-3. Epub 2011 Aug 11.
This study investigated the influence of lifestyle on aging-related changes in cardiac proteins' oxidative modifications profile. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young Y, old sedentary S, and old active A). The S and A mice were individually placed into standard cages and in cages with running wheels, respectively, for 23 months. Upon killing, heart mitochondrial fractions were obtained for the evaluation of general proteins oxidative modifications profile, the identification of preferential protein targets, and oxidative phosphorylation (OXPHOS) activity. We observed age-related cardiac muscle impairment, evidenced by decreased OXPHOS activity, paralleled by an increased protein susceptibility to carbonylation and nitration. Among the main targets to these posttranslational modifications we found mitochondrial proteins, mainly from OXPHOS complexes, MnSOD and enzymes from lipid metabolism. Lifelong sedentary behavior exacerbated the nitrative damage of mitochondrial proteins, paralleled by a statistically significant decrease of respiratory chain complexes II and III activities. In overall, our results highlight the determinant role of aging in cardiac muscle impairment, which is worsened by a sedentary lifestyle.
本研究调查了生活方式对与衰老相关的心脏蛋白氧化修饰谱变化的影响。30 只 C57BL/6 品系小鼠（2 个月）被随机分为三组（年轻 Y 组、老年久坐 S 组和老年活跃 A 组）。S 和 A 组小鼠分别被单独放入标准笼和带跑轮的笼中，持续 23 个月。处死时，获取心脏线粒体部分，用于评估总蛋白氧化修饰谱、鉴定优先蛋白靶标和氧化磷酸化（OXPHOS）活性。我们观察到与年龄相关的心肌损伤，表现为 OXPHOS 活性降低，同时蛋白易发生羰基化和硝化。在这些翻译后修饰的主要靶标中，我们发现了线粒体蛋白，主要来自 OXPHOS 复合物、MnSOD 和脂质代谢酶。终身久坐行为加剧了线粒体蛋白的硝化损伤，同时呼吸链复合物 II 和 III 的活性显著下降。总的来说，我们的结果强调了衰老在心肌损伤中的决定性作用，而久坐的生活方式会使其恶化。
