微粒体谷胱甘肽依赖性不稳定因子对脂质过氧化的保护作用。

Protection against lipid peroxidation by a microsomal glutathione-dependent labile factor.

作者信息

Haenen G R, Bast A

出版信息

FEBS Lett. 1983 Aug 8;159(1-2):24-8. doi: 10.1016/0014-5793(83)80409-8.

Abstract

Glutathione (GSH) protects rat liver microsomes against ascorbic acid (0.2 mM)/ferrous iron (10 microM)-induced lipid peroxidation for some time. The inhibitory effect of GSH is concentration-dependent (0.1-1.0 mM). Our data suggest that GSH acts by preventing initial radical formation rather than via radical scavenging or GSH--peroxidase activity. A labile GSH-dependent factor is involved in the inhibition of microsomal lipid peroxidation by GSH, inasmuch as heating the microsomes abolishes the GSH effect. We found that besides heating, lipid peroxidation also destroys the GSH-dependent factor. Consequently, continuous radical stress will produce lipid peroxidation, despite the presence of GSH. Moreover, a detrimental effect of in vivo-induced lipid peroxidation (CCl4-treatment) on the GSH-dependent factor was observed. The implications of the present data for the genesis of and the protection against peroxidative damage are discussed.

摘要

谷胱甘肽（GSH）可在一段时间内保护大鼠肝微粒体免受抗坏血酸（0.2 mM）/亚铁离子（10 microM）诱导的脂质过氧化作用。GSH的抑制作用呈浓度依赖性（0.1 - 1.0 mM）。我们的数据表明，GSH的作用机制是阻止初始自由基的形成，而非通过自由基清除或谷胱甘肽过氧化物酶活性。一种不稳定的GSH依赖性因子参与了GSH对微粒体脂质过氧化的抑制作用，因为加热微粒体会消除GSH的作用。我们发现，除了加热，脂质过氧化也会破坏GSH依赖性因子。因此，尽管存在GSH，持续的自由基应激仍会产生脂质过氧化。此外，还观察到体内诱导的脂质过氧化（CCl4处理）对GSH依赖性因子有有害影响。本文讨论了这些数据对过氧化损伤的发生及防护的意义。