Department of Biochemistry, Molecular Biology, and Biophysics, The University of Minnesota-Twin Cities, Minneapolis, MN 55455, USA.
Trends Endocrinol Metab. 2012 Aug;23(8):399-406. doi: 10.1016/j.tem.2012.05.008. Epub 2012 Jun 27.
Oxidative stress is linked to the production of reactive lipid aldehydes that non-enzymatically alkylate cysteine, histidine, or lysine residues in a reaction termed protein carbonylation. Reactive lipid aldehydes and their derivatives are detoxified via a variety of phase I and phase II systems, and when antioxidant defenses are compromised or oxidative conditions are increased, protein carbonylation is increased. The resulting modification has been implicated as causative in a variety of metabolic states including neurodegeneration, muscle wasting, insulin resistance, and aging. Although such modifications usually result in loss of protein function, protein carbonylation may be regulatory and activate signaling pathways involved in antioxidant biology and cellular homeostasis.
氧化应激与反应性脂质醛的产生有关，这些脂质醛通过一种称为蛋白质羰基化的反应非酶促地烷基化半胱氨酸、组氨酸或赖氨酸残基。反应性脂质醛及其衍生物通过各种 I 相和 II 相系统解毒，当抗氧化防御受损或氧化条件增加时，蛋白质羰基化增加。这种修饰被认为是多种代谢状态的原因，包括神经退行性变、肌肉减少、胰岛素抵抗和衰老。尽管这种修饰通常导致蛋白质功能丧失，但蛋白质羰基化可能具有调节作用，并激活参与抗氧化生物学和细胞内稳态的信号通路。
