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氧自由基介导紫外线对线粒体膜的损伤作用。

Oxygen free-radicals mediate the damaging effect of ultraviolet light on membrane mitochondria.

作者信息

Chávez E, Zazueta C, Cuéllar A, Reyes-Vivas H, García N

机构信息

Departamento de Bioquímica, Instituto Nacional de Cardiología, Ignacio Chávez, México, D.F., México.

出版信息

Biochem Mol Biol Int. 1998 Sep;46(1):207-14. doi: 10.1080/15216549800203712.

DOI:10.1080/15216549800203712
PMID:9784855
Abstract

This paper reports evidence that exposure of mitochondria to near-ultraviolet light inhibits electron transport, collapses the electric gradient, and increases non-specific membrane permeability to matrix solutes such as Ca2+. Membrane energization, as well as superoxide dismutase and catalase avoid membrane leakiness. Increased permeability correlates with a diminution in the titrated thiol groups. Plausibly the pore is formed through the formation of sulfhydryl bridges by the action of UV light-derived oxygen-centered free- radicals on membrane proteins.

摘要

本文报道了以下证据

线粒体暴露于近紫外线下会抑制电子传递、破坏电化学梯度,并增加对基质溶质(如Ca2+)的非特异性膜通透性。膜的能量化以及超氧化物歧化酶和过氧化氢酶可避免膜渗漏。通透性增加与滴定的巯基减少相关。推测该孔是由紫外线衍生的以氧为中心的自由基作用于膜蛋白形成巯基桥而形成的。

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