Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN, USA.
Adv Nutr. 2013 Mar 1;4(2):157-63. doi: 10.3945/an.112.003319.
Oxidative stress has been identified as a common mechanism for cellular damage and dysfunction in a wide variety of disease states. Current understanding of the metabolic changes associated with obesity and the development of insulin resistance has focused on the role of oxidative stress and its interaction with inflammatory processes at both the tissue and organismal level. Obesity-related oxidative stress is an important contributing factor in the development of insulin resistance in the adipocyte as well as the myocyte. Moreover, oxidative stress has been linked to mitochondrial dysfunction, and this is thought to play a role in the metabolic defects associated with oxidative stress. Of the various effects of oxidative stress, protein carbonylation has been identified as a potential mechanism underlying mitochondrial dysfunction. As such, this review focuses on the relationship between protein carbonylation and mitochondrial biology and addresses those features that point to either the causal or casual relationship of lipid peroxidation-induced protein carbonylation as a determining factor in mitochondrial dysfunction.
氧化应激已被确定为多种疾病状态下细胞损伤和功能障碍的共同机制。目前对肥胖相关代谢变化以及胰岛素抵抗发展的理解主要集中在氧化应激的作用及其与组织和机体水平炎症过程的相互作用上。肥胖相关的氧化应激是脂肪细胞和肌细胞中胰岛素抵抗发展的一个重要因素。此外，氧化应激与线粒体功能障碍有关，这被认为与氧化应激相关的代谢缺陷有关。在氧化应激的各种影响中，蛋白质羰基化已被确定为线粒体功能障碍的潜在机制。因此，本综述重点关注蛋白质羰基化与线粒体生物学之间的关系，并探讨了那些指向脂质过氧化诱导的蛋白质羰基化作为线粒体功能障碍决定因素的因果关系或偶然关系的特征。
