Kowaltowski A J, Vercesi A E
Departamento de Patologia Clínica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, SP, Brazil.
Free Radic Biol Med. 1999 Feb;26(3-4):463-71. doi: 10.1016/s0891-5849(98)00216-0.
Up to 2% of the oxygen consumed by the mitochondrial respiratory chain undergoes one electron reduction, typically by the semiquinone form of coenzyme Q, to generate the superoxide radical, and subsequently other reactive oxygen species such as hydrogen peroxide and the hydroxyl radical. Under conditions in which mitochondrial generation of reactive oxygen species is increased (such as in the presence of Ca2+ ions or when the mitochondrial antioxidant defense mechanisms are compromised), these reactive oxygen species may lead to irreversible damage of mitochondrial DNA, membrane lipids and proteins, resulting in mitochondrial dysfunction and ultimately cell death. The nature of this damage and the cellular conditions in which it occurs are discussed in this review article.
线粒体呼吸链消耗的氧气中,高达2%会经历单电子还原,通常是通过辅酶Q的半醌形式,生成超氧阴离子自由基,随后还会生成其他活性氧物种,如过氧化氢和羟基自由基。在活性氧物种的线粒体生成增加的情况下(例如存在Ca2+离子时或线粒体抗氧化防御机制受损时),这些活性氧物种可能导致线粒体DNA、膜脂和蛋白质的不可逆损伤,从而导致线粒体功能障碍并最终导致细胞死亡。本文综述了这种损伤的性质及其发生的细胞条件。