LIPID-PEROXIDATION IN CATARACT OF THE HUMAN
LIPID-PEROXIDATION IN CATARACT OF THE HUMAN
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DOI：
10.1016/0024-3205(86)90559-x
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发表时间：
1986-04-21
期刊：
影响因子：
6.1
通讯作者：
PODOS, SM
中科院分区：
文献类型：
--
作者：
BHUYAN, KC;BHUYAN, DK;PODOS, SM
脂质过氧化是人类白内障发生的可能机制之一。丙二醛（MDA），脂质过氧化物的主要分解产物，显着高于在正常晶状体相比，在白内障晶状体。2-从皮质性白内障中分离并经SephadexG-10柱层析纯化的硫代巴比妥酸反应物质被鉴定为MDA。在白内障晶状体的酶防御反应物种的O2受损的超氧化物歧化酶，过氧化氢酶和谷胱甘肽过氧化物酶的活性显着下降。与白内障相关的人眼的房水和玻璃体液中的过氧化氢增加2-3倍。MDA的羰基可能与晶状体质膜蛋白质和磷脂的伯氨基发生交联反应，形成席夫碱结合物，从而参与白内障的发病机制。
Lipid peroxidation was investigated as one of the possible mechanisms of cataractogenesis in the human. Malondialdehyde (MDA), a major breakdown product of lipid peroxides, was significantly higher in cataractous lenses as compared to that in normal lenses. 2-Thiobarbituric acid-reactive material, isolated from cortical cataracts and purified by Sephadex G-10 column chromatography, was identified as MDA. In cataractous lenses the enzymic defenses against reactive species of O2 were impaired as evidenced by the significant decrease in activities of superoxide dismutase, catalase and glutathione peroxidase. Hydrogen peroxide in aqueous humor and vitreous humor of human eyes associated with cataract was increased 2-3 fold. It is possible that carbonyl groups of MDA could interact with primary amino groups of proteins and phospholipids of lenticular plasmalemmae by a cross-linking reaction forming Schiff-base conjugates and these mechanisms might be involved in the pathogenesis of cataract.