Stadtman E R, Levine R L
Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-0320, USA.
Ann N Y Acad Sci. 2000;899:191-208. doi: 10.1111/j.1749-6632.2000.tb06187.x.
The oxidative modification of proteins by reactive species, especially reactive oxygen species, is implicated in the etiology or progression of a panoply of disorders and diseases. These reactive species form through a large number of physiological and non-physiological reactions. An increase in the rate of their production or a decrease in their rate of scavenging will increase the oxidative modification of cellular molecules, including proteins. For the most part, oxidatively modified proteins are not repaired and must be removed by proteolytic degradation, and a decrease in the efficiency of proteolysis will cause an increase in the cellular content of oxidatively modified proteins. The level of these modified molecules can be quantitated by measurement of the protein carbonyl content, which has been shown to increase in a variety of diseases and processes, most notably during aging. Accumulation of modified proteins disrupts cellular function either by loss of catalytic and structural integrity or by interruption of regulatory pathways.
活性物质，尤其是活性氧对蛋白质的氧化修饰，与一系列疾病和病症的病因或进展有关。这些活性物质通过大量生理和非生理反应形成。其产生速率的增加或清除速率的降低会增加细胞分子（包括蛋白质）的氧化修饰。在大多数情况下，氧化修饰的蛋白质无法修复，必须通过蛋白水解降解来清除，而蛋白水解效率的降低会导致氧化修饰蛋白质的细胞含量增加。这些修饰分子的水平可以通过测量蛋白质羰基含量来定量，蛋白质羰基含量已被证明在多种疾病和过程中会增加，最显著的是在衰老过程中。修饰蛋白质的积累会通过催化和结构完整性的丧失或调节途径的中断来破坏细胞功能。
