Robison W G, Kuwabara T, Bieri J G
Laboratory of Vision Research, National Eye Institute, National Institutes of Health, Bethesda, Maryland, MD 20205.
Retina. 1982;2(4):263-81.
Relatively high proportions of long-chain, polyunsaturated fatty acids seem to be required in rod photoreceptor membranes in order to provide the precise microenvironment for the proper function of the visual pigment rhodopsin. At the same time, such high levels of lipid unsaturation put the photoreceptor membranes at a high risk for autoxidation. The antioxidant vitamin E which can minimize autoxidation of polyunsaturated fatty acids is found in rather high concentrations in the outer segment membranes. Dietary deficiency in vitamin E induces disintegration of rod outer segment membranes, probably by increasing autoxidation. Also, it greatly accelerates the accumulation of aging pigments in the retinal pigment epithelium, probably because these lipofuscin granules do indeed represent the end products of lipid peroxidation. Vitamin E supplements, up to threefold normal levels, appear to provide no significant protection of the retina from light damage produced either by short but acute or by long-term, low level exposures to light. This is not consistent with current theories which implicate lipid peroxidation in the destruction of rod outer segments in light damaged retinas; more work is needed before any relation between retinal light damage and vitamin E levels can be assessed. Surprisingly, the amount of lipofuscin granule accumulation in the retinal pigment epithelium is influenced dramatically by dietary levels of vitamin A. Even retinas lacking a source of polyunsaturated fatty acids from rod outer segments still may accumulate massive lipofuscin if dietary vitamin A is provided. Perhaps vitamin A, which has such a dynamic relationship with the retinal pigment epithelium, becomes oxidized, and then contributes to the formation of a lipofuscin-like pigment. Centrophenoxine, a drug claimed to be effective in reversing the accumulation of age-related lipofuscin in the central nervous system, has no obvious effect in the eye or uterus in removing the lipofuscin granules induced by vitamin E deficiency. Microperoxisomes are abundant in the retinal pigment epithelium, and may be associated with rapid lipid turnover and/or utilization of lipid soluble vitamins. Their potential roles, however, need further documentation and clarification. Recently developed techniques and new discoveries in lipid research open the way for many fruitful studies on the interactions and precise roles of lipids and lipid-soluble vitamins in vision.
视杆光感受器膜似乎需要相对较高比例的长链多不饱和脂肪酸，以便为视色素视紫红质的正常功能提供精确的微环境。与此同时，如此高的脂质不饱和度使光感受器膜面临自氧化的高风险。能够使多不饱和脂肪酸自氧化最小化的抗氧化剂维生素E在外段膜中含量相当高。饮食中维生素E缺乏会导致视杆外段膜解体，可能是通过增加自氧化作用。此外，它还会极大地加速视网膜色素上皮中衰老色素的积累，可能是因为这些脂褐素颗粒确实代表脂质过氧化的终产物。维生素E补充剂，达到正常水平的三倍，似乎并不能显著保护视网膜免受短期急性或长期低水平光照产生的光损伤。这与目前认为脂质过氧化参与光损伤视网膜中视杆外段破坏的理论不一致；在评估视网膜光损伤与维生素E水平之间的任何关系之前，还需要更多的研究。令人惊讶的是，视网膜色素上皮中脂褐素颗粒的积累量受到饮食中维生素A水平的显著影响。即使视网膜缺乏来自视杆外段的多不饱和脂肪酸来源，但如果提供饮食中的维生素A，仍然可能积累大量脂褐素。也许与视网膜色素上皮有如此动态关系的维生素A会被氧化，然后有助于形成类似脂褐素的色素。环扁桃酯，一种据称对逆转中枢神经系统中与年龄相关的脂褐素积累有效的药物，在眼睛或子宫中对消除维生素E缺乏诱导的脂褐素颗粒没有明显效果。微过氧化物酶体在视网膜色素上皮中丰富，可能与脂质的快速周转和/或脂溶性维生素的利用有关。然而，它们的潜在作用需要进一步的记录和阐明。最近在脂质研究中开发的技术和新发现为许多关于脂质和脂溶性维生素在视觉中的相互作用和精确作用的富有成果的研究开辟了道路。
