Nalini S, Balasubramanian K A
Wellcome Research Unit, Christian Medical College Hospital, Vellore, India.
Chem Biol Interact. 1991;80(2):135-44. doi: 10.1016/0009-2797(91)90020-8.
Rat liver and intestinal microsomes were exposed to various free radical generating systems and their effect were assessed by studying different parameters such as formation of malonaldehyde (MDA) and conjugated diene, arachidonic acid depletion and alteration in protein thiol groups and tocopherol levels. These studies revealed that liver being highly vulnerable tissue showed all the effects of free radical attack whereas intestinal microsomes were resistant to most oxidants except iron independent generation of free radicals using 2-2'-azobis (2-amidinopropane) dihydrochloride (ABAP). Intestinal microsomes were found to contain considerable amount of non-esterified fatty acids in total lipid fraction as compared to liver microsomes and iron-fatty acid complex may be incapable of participating in peroxidation. In vitro measurement of hydroxyl radical generation showed that intestinal microsomes were incapable of generating these active species. These results suggest that iron dependent free radical mediated lipid peroxidation might not occur in intestinal epithelial cells.
将大鼠肝脏和肠道微粒体暴露于各种自由基生成系统，并通过研究不同参数来评估其效果，如丙二醛（MDA）和共轭二烯的形成、花生四烯酸的消耗以及蛋白质硫醇基团和生育酚水平的变化。这些研究表明，肝脏作为高度易损组织，表现出自由基攻击的所有效应，而肠道微粒体对大多数氧化剂具有抗性，但使用2-2'-偶氮二（2-脒基丙烷）二盐酸盐（ABAP）进行的不依赖铁的自由基生成除外。与肝脏微粒体相比，发现肠道微粒体在总脂质部分中含有相当数量的非酯化脂肪酸，并且铁-脂肪酸复合物可能无法参与过氧化反应。体外测量羟基自由基的生成表明，肠道微粒体无法生成这些活性物质。这些结果表明，铁依赖性自由基介导的脂质过氧化可能不会在肠道上皮细胞中发生。
