Nagasaka Y, Fujii S, Kaneko T
Third Department of Internal Medicine, Yamaguchi University, School of Medicine, Japan.
Arch Biochem Biophys. 1989 Oct;274(1):82-6. doi: 10.1016/0003-9861(89)90417-7.
Ascorbate-Fe3+-induced and NADPH-induced lipid peroxidation of rat liver microsomes were inhibited by glutathione (GSH). This inhibition was due to microsomal GSH-dependent factor. This factor was heat labile, and storage of microsomes at 4 degrees C for 1 week diminished the activity. GSH could not be substituted by other sulfhydryl compounds tested. Deoxycholate (1 mM) and bromosulfophthalein (0.1 mM) inhibited GSH-dependent protection but did not inhibit microsomal GSH peroxidase activity. Iodoacetate (10 mM) inhibited GSH-dependent protection but did not inhibit microsomal GSH S-transferase. N-Ethylmaleimide (0.1 mM) and oxidized glutathione (10 mM) inhibited GSH-dependent protection but activated microsomal GSH S-transferase activity. These results indicate the existence of a heat-labile, microsomal GSH-dependent protective factor against lipid peroxidation that acts through a factor other than GSH-peroxidase and GSH S-transferase.
谷胱甘肽（GSH）可抑制抗坏血酸盐 - 铁离子诱导的以及NADPH诱导的大鼠肝微粒体脂质过氧化。这种抑制作用归因于微粒体中依赖GSH的因子。该因子对热不稳定，微粒体在4℃储存1周会使其活性降低。所测试的其他巯基化合物不能替代GSH。脱氧胆酸盐（1 mM）和溴磺酞（0.1 mM）可抑制依赖GSH的保护作用，但不抑制微粒体GSH过氧化物酶活性。碘乙酸盐（10 mM）抑制依赖GSH的保护作用，但不抑制微粒体GSH S - 转移酶。N - 乙基马来酰亚胺（0.1 mM）和氧化型谷胱甘肽（10 mM）抑制依赖GSH的保护作用，但激活微粒体GSH S - 转移酶活性。这些结果表明存在一种对脂质过氧化具有保护作用的、热不稳定的、微粒体中依赖GSH的因子，其作用途径不同于GSH过氧化物酶和GSH S - 转移酶。
Zotero 插件