Bhuyan K C, Bhuyan D K, Podos S M
Life Sci. 1986 Apr 21;38(16):1463-71. doi: 10.1016/0024-3205(86)90559-x.
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.
脂质过氧化作为人类白内障形成的可能机制之一进行了研究。脂质过氧化物的主要分解产物丙二醛（MDA）在白内障晶状体中显著高于正常晶状体。从皮质性白内障中分离并通过葡聚糖凝胶G - 10柱色谱法纯化的2 - 硫代巴比妥酸反应性物质被鉴定为MDA。在白内障晶状体中，超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性显著降低，这表明对活性氧物种的酶防御受损。与白内障相关的人眼房水和玻璃体液中的过氧化氢增加了2 - 3倍。MDA的羰基可能通过交联反应与晶状体质膜的蛋白质和磷脂的伯氨基相互作用，形成席夫碱共轭物，这些机制可能参与了白内障的发病过程。
