Corbucci G G, Gasparetto A, Antonelli M, Bufi M, De Blasi R A
Int J Tissue React. 1986;8(5):421-30.
Following our previous findings on mitochondrial oxidative damage during the course of circulatory shock in human muscular tissue, in the present work we examined the pathogenic connections between the electron-transport-chain enzymic activity and the ubiquinone metabolism. The effects of the oxidative damage on the alpha-tocopherol content and malondialdehyde (MDA) levels were also studied. The results reveal an involvement of cytochrome oxidase and coenzyme Q10 in the oxidative damage due to shock; alpha-tocopherol seems to show a particularly increased antioxidant activity contemporary with the marked increase in MDA levels. These findings suggest that the significant fall in the mitochondrial oxidative capacity could generate an oxygen free-radical production with subsequent peroxidative damage of the mitochondrial inner-membrane bilayer.
基于我们之前关于人类肌肉组织循环性休克过程中线粒体氧化损伤的研究结果,在本研究中,我们探讨了电子传递链酶活性与泛醌代谢之间的致病联系。同时还研究了氧化损伤对α-生育酚含量和丙二醛(MDA)水平的影响。结果表明,细胞色素氧化酶和辅酶Q10参与了休克引起的氧化损伤;在MDA水平显著升高的同时,α-生育酚似乎表现出特别增强的抗氧化活性。这些发现表明,线粒体氧化能力的显著下降可能会产生氧自由基,随后导致线粒体内膜双层的过氧化损伤。