Remé C E, Malnoë A, Jung H H, Wei Q, Munz K
University Eye Clinic, Zürich, Switzerland.
Invest Ophthalmol Vis Sci. 1994 Jan;35(1):78-90.
Previous studies have shown that ingestion of fish oil (FO) containing a high proportion of n-3 polyunsaturated fatty acids increases the susceptibility of cellular membranes to oxidative damage in various tissues. In the retina, lipid peroxidation is thought to be a major mechanism contributing to light-induced lesions. Therefore, we investigated the effect of FO on acute light-induced photoreceptor damage.
For 2 months, weanling rats were fed diets containing either soybean oil (SOY) or FO as main lipid component.
Rats fed FO had significantly higher levels of eicosapentaenoic acid (EPA, 20:5n-3) and higher ratios of EPA to arachidonic acid (AA, 20:4n-6) in retinal phospholipids and diacylglycerols than rats fed SOY. The levels of docosahexaenoic acid (DHA, 22:6n-3) were similar in both dietary groups. The susceptibility to lipid peroxidation was enhanced in the isolated retina of FO-fed rats as shown by higher levels of thiobarbituric acid reactive substances after incubation of retinal membranes with Fe2+/ascorbate. The retinal content of alpha-tocopherol was similar in SOY- and FO-fed animals. Light damage consisting of acute rod outer segment (ROS) disruptions was induced by exposing dark-adapted animals to 600 to 700 lux (230 to 260 microW/cm2) of white fluorescent light for 30 minutes. Damage was quantitated using a computerized multifunctional image analysis of retinal thin sections. Although structural alterations of the ROS were present in both groups, FO-fed rats showed less damage at the base of the ROS. This occurred in spite of higher rhodopsin levels in FO-fed rats. There was no effect of diet on retinal morphology in dark-adapted rats.
These results indicate that FO does not enhance the susceptibility to acute ROS disk disruptions in the rat retina. Our study further suggests that FO exerts a partial protective effect that may be related to changes in the formation of lipid mediators derived from EPA and AA in retinal phospholipids.
先前的研究表明，摄入富含n-3多不饱和脂肪酸的鱼油（FO）会增加各种组织中细胞膜对氧化损伤的易感性。在视网膜中，脂质过氧化被认为是导致光诱导损伤的主要机制。因此，我们研究了鱼油对急性光诱导的光感受器损伤的影响。
将断奶大鼠以大豆油（SOY）或鱼油作为主要脂质成分喂养2个月。
与喂食大豆油的大鼠相比，喂食鱼油的大鼠视网膜磷脂和二酰基甘油中的二十碳五烯酸（EPA，20:5n-3）水平显著更高，且EPA与花生四烯酸（AA，20:4n-6）的比例更高。两个饮食组中的二十二碳六烯酸（DHA，22:6n-3）水平相似。在用Fe2+/抗坏血酸孵育视网膜膜后，喂食鱼油的大鼠分离视网膜中脂质过氧化的易感性增强，表现为硫代巴比妥酸反应性物质水平更高。喂食大豆油和鱼油的动物视网膜中α-生育酚含量相似。通过将暗适应的动物暴露于600至700勒克斯（230至260微瓦/平方厘米）的白色荧光灯下30分钟，诱导出由急性视杆细胞外段（ROS）破坏组成的光损伤。使用视网膜薄片的计算机化多功能图像分析对损伤进行定量。尽管两组均存在ROS的结构改变，但喂食鱼油的大鼠在ROS基部的损伤较小。尽管喂食鱼油的大鼠视紫红质水平较高，但仍出现这种情况。饮食对暗适应大鼠的视网膜形态没有影响。
这些结果表明，鱼油不会增强大鼠视网膜对急性ROS盘破坏的易感性。我们的研究进一步表明，鱼油发挥了部分保护作用，这可能与视网膜磷脂中源自EPA和AA的脂质介质形成变化有关。
