Babizhayev M A, Deyev A I, Linberg L F
Moscow Helmholtz Eye Diseases Research Institute, U.S.S.R.
Mech Ageing Dev. 1988 Jul;44(1):69-89. doi: 10.1016/0047-6374(88)90080-2.
The role of free-radical-induced lipid oxidation in the development of human lens opacity was studied. Physico-chemical parameters of the lens fiber membranes at different stages of cataract have been investigated. The deterioration of lens fiber plasma membranes structure preceding formation of large aggregates in lenticular matter, leading to lens opacity, was observed by electron microscopy. Initial stages of cataract were characterized by the accumulation of primary (diene conjugates, cetodienes) lipid peroxidation (LPO) products, while in the later stages there was a prevalence of end LPO fluorescent products. Reliable increase in oxiproducts of fatty acyl content of lenticular lipids was shown by direct gas chromatography technique obtaining fatty acid fluorine-substituted derivatives. The lens opacity degree is found to correlate with the level of the end LPO fluorescent product accumulation in its tissue, accompanied by SH group oxidation of crystallins due to decrease of reduced glutathione concentration in the lens. The injection of LPO products into the vitreous has been shown to induce cataract. It was concluded that peroxide damage of the lens fiber membranes may be the initiatory cause of cataract development.
研究了自由基诱导的脂质氧化在人晶状体混浊发展中的作用。研究了白内障不同阶段晶状体纤维膜的物理化学参数。通过电子显微镜观察到,在晶状体物质中形成大聚集体导致晶状体混浊之前,晶状体纤维质膜结构的恶化。白内障的初始阶段以初级(二烯共轭物、鲸蜡二烯)脂质过氧化(LPO)产物的积累为特征,而在后期,末端LPO荧光产物占主导。通过直接气相色谱技术获得脂肪酸氟取代衍生物,显示晶状体脂质的脂肪酰基含量的氧化产物可靠增加。发现晶状体混浊程度与其组织中末端LPO荧光产物积累水平相关,同时由于晶状体中还原型谷胱甘肽浓度降低,晶状体蛋白的SH基团发生氧化。已证明向玻璃体注射LPO产物可诱发白内障。得出的结论是,晶状体纤维膜的过氧化物损伤可能是白内障发展的起始原因。