Paradies G, Ruggiero F M, Petrosillo G, Quagliariello E
Department of Biochemistry and Molecular Biology, University of Bari, Italy.
FEBS Lett. 1998 Mar 13;424(3):155-8. doi: 10.1016/s0014-5793(98)00161-6.
Rat heart mitochondrial membranes exposed to the free radicals generating system tert-butylhydroperoxide/Cu2+ undergo lipid peroxidation as evidenced by the accumulation of thyobarbituric acid reactive substances. Mitochondrial lipid peroxidation resulted in a marked loss of both cytochrome c oxidase activity and cardiolipin content. The alterations in the properties of cytochrome c oxidase were confined to a decrease in the maximal activity (Vmax) with no change in the affinity (Km) with respect to the substrate cytochrome c. Various lipid soluble antioxidants could prevent the lipid peroxidation reaction and the associated loss of cytochrome c oxidase activity. External added cardiolipin but no other phospholipids, nor peroxidized cardiolipin was able to prevent the loss of cytochrome oxidase activity induced by lipid peroxidation. These results establish a close correlation between oxidative damage to cardiolipin and alterations in the cytochrome oxidase activity and may prove useful in probing molecular mechanism of free radicals induced peroxidative damage of mitochondria which has been proposed to contribute to aging and to chronic degenerative diseases.
暴露于自由基生成系统叔丁基过氧化氢/Cu2+的大鼠心脏线粒体膜会发生脂质过氧化，这可通过硫代巴比妥酸反应性物质的积累得到证明。线粒体脂质过氧化导致细胞色素c氧化酶活性和心磷脂含量显著降低。细胞色素c氧化酶性质的改变仅限于最大活性（Vmax）降低，而对底物细胞色素c的亲和力（Km）没有变化。各种脂溶性抗氧化剂可以防止脂质过氧化反应以及相关的细胞色素c氧化酶活性丧失。外部添加的心磷脂，但不是其他磷脂，也不是过氧化的心磷脂，能够防止脂质过氧化诱导的细胞色素氧化酶活性丧失。这些结果建立了心磷脂氧化损伤与细胞色素氧化酶活性改变之间的密切相关性，并且可能有助于探索自由基诱导的线粒体过氧化损伤的分子机制，这种损伤被认为与衰老和慢性退行性疾病有关。
