Konat G, Gantt G, Gorman A, Wiggins R C
Department of Neurology, Medical University of South Carolina, Charleston 29425.
Metab Brain Dis. 1986 Sep;1(3):177-85. doi: 10.1007/BF01001779.
The exposure of CNS myelin to reactive oxygen species (ROS) generated by a Cu2+-H2O2 system results in the aggregation of membrane proteins. Integral and peripheral membrane proteins are equally vulnerable and the denaturation is not mediated by the SH groups. The aggregated proteins retain their original antigenicity as determined by immunoblot technique. The aggregation of proteins is not limited to myelin and can be elicited in the preparation of other cerebral membranes. The effect of ROS on membrane proteins can also be demonstrated in cerebral slices incubated in the presence of the ROS-generating system. Furthermore, the peroxidation inactivates membrane-bound enzymes as exemplified by myelin cyclic nucleotide phosphatase (CNP). Competitive inhibition studies with various scavengers and quenchers of ROS implicate singlet oxygen as a major mediator in the Cu2+-H2O2 oxidizing system responsible for the peroxidative aggregation of membrane proteins.
中枢神经系统髓磷脂暴露于由铜离子 - 过氧化氢系统产生的活性氧(ROS)会导致膜蛋白聚集。整合膜蛋白和外周膜蛋白同样易受影响,且变性并非由巯基介导。通过免疫印迹技术测定,聚集的蛋白保留了其原始抗原性。蛋白聚集并不局限于髓磷脂,在制备其他脑膜时也可引发。在存在活性氧生成系统的情况下孵育的脑片中,也可证明活性氧对膜蛋白的影响。此外,过氧化作用会使膜结合酶失活,髓磷脂环核苷酸磷酸酶(CNP)就是一个例子。用各种活性氧清除剂和猝灭剂进行的竞争性抑制研究表明,单线态氧是铜离子 - 过氧化氢氧化系统中负责膜蛋白过氧化聚集的主要介质。