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叔丁基过氧化氢作用下大鼠红细胞的膜形态、磷脂和细胞骨架蛋白的恶化:在硒缺乏时外源性谷胱甘肽的保护作用失效

Deterioration of membrane morphology, phospholipids, and cytoskeletal protein in rat erythrocytes exposed to tert-butyl hydroperoxide: protection by exogenous glutathione fails in selenium deficiency.

作者信息

Suzuki T, Kim C H, Yasumoto K

机构信息

Research Institute for Food Science, Kyoto University, Japan.

出版信息

J Nutr Sci Vitaminol (Tokyo). 1988 Oct;34(5):491-506. doi: 10.3177/jnsv.34.491.

Abstract

Here we report scanning electron microscopy, phospholipid and fatty acid composition and cytoskeleton proteins of erythrocytes from Se-adequate and Se-deficient rats, showing protection by glutathione (GSH) against tert-butyl hydroperoxide (t-BuOOH)-induced hemolysis of erythrocytes from Se-adequate, but not from Se-deficient rats. Without exogenous GSH, erythrocytes incubated with t-BuOOH exhibited remarkable deterioration of cell membranes with diminished membrane phosphatidyl-ethanolamine, -serine, and -inositol and selective loss of a cytoskeletal protein, ankyrin 2-1. Without exogenous GSH these changes occurred in erythrocytes from both Se-deficient and Se-adequate rats. Dietary Se, through provision of glutathione peroxidase (GSH-Px) in erythrocytes as a probable scavenger of t-BuOOH, protects against hemolysis when GSH is available.

摘要

在此,我们报告了来自硒充足和硒缺乏大鼠的红细胞的扫描电子显微镜、磷脂和脂肪酸组成以及细胞骨架蛋白,结果显示谷胱甘肽(GSH)可保护硒充足大鼠的红细胞免受叔丁基过氧化氢(t-BuOOH)诱导的溶血,但对硒缺乏大鼠的红细胞无此保护作用。在没有外源性GSH的情况下,与t-BuOOH孵育的红细胞表现出细胞膜明显恶化,膜磷脂酰乙醇胺、丝氨酸和肌醇减少,以及一种细胞骨架蛋白锚蛋白2-1的选择性丢失。在没有外源性GSH的情况下,硒缺乏和硒充足大鼠的红细胞均出现这些变化。膳食硒通过在红细胞中提供谷胱甘肽过氧化物酶(GSH-Px)作为t-BuOOH的可能清除剂,在有GSH时可防止溶血。

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