Deficiencies of vitamins E and A in the rat. Retinal damage and lipofuscin accumulation.
Deficiencies of vitamins E and A in the rat. Retinal damage and lipofuscin accumulation.
复制标题
大鼠缺乏维生素E和A。
DOI：
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发表时间：
1980
影响因子：
4.4
通讯作者：
J. G. Bieri
中科院分区：
文献类型：
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作者：
W. Robison;T. Kuwabara;J. G. Bieri
在四组断奶雌性大鼠中研究了维生素 E 和 A 在维持视网膜各种结构成分方面的相互关系，这些大鼠喂食的纯化饮食中每种维生素充足或缺乏：+E、+A； -E，+A； +E，-A；和-E、-A。缺乏视黄醇(-A)的组补充视黄酸。 14、21和35周后，对视网膜进行组织学和超微结构检查。 35周时，双缺陷大鼠（-E，-A）失去了92％的视杆细胞核，而缺乏维生素A（+E，-A）或单独缺乏维生素E（-E，+A）的大鼠仅分别损失了34％和20％。维生素 E 缺乏早在 21 周时就导致视网膜色素上皮中出现广泛的脂褐素沉积，但维生素 A 的存在使脂褐素颗粒的数量增加了一倍（-E、+A 与 -E、-A），并诱导其自发荧光的增加甚至更大。维生素A的另一个明显影响是，当+E、+A视网膜自发荧光不仅比+E、-A视网膜（其颗粒数量相似）多得多，而且还多于-E、-A视网膜（其脂褐质颗粒数量大约是-E、-A视网膜的两倍）时。在视网膜中，与子宫不同，脂褐素特异性自发荧光和脂褐素颗粒数量不成比例。此外，颗粒的数量同时受到维生素 E 和 A 的影响，而脂褐素特异性自发荧光的强度几乎完全由维生素 A 决定。在缺乏维生素 E 保护的情况下，-E、-A 视网膜中感光细胞的加速损失可能是由膜的氧化和视网膜维生素 A 储存的氧化造成的。
The interrelationships of vitamins E and A in maintaining various structural components of the retina were studied in four groups of weanling female rats fed purified diets adequate or deficient in each vitamin: +E, +A; -E, +A; +E, -A; and -E, -A. Groups deficient in retinol (-A) were supplemented with retinoic acid. After 14, 21, and 35 weeks, the retinas were examined histologically and ultrastructurally. At 35 weeks, the doubly deficient rats (-E, -A) had lost 92% of their rod nuclei, whereas rats deficient in vitamins A (+E, -A) or E (-E, +A) alone had lost only 34% and 20%, respectively. Vitamin E deficiency resulted in extensive lipofuscin deposits in the retinal pigment epithelium as early as 21 weeks, but the presence of vitamin A doubled the number of lipofuscin granules (-E, +A vs. -E, -A) and induced an even greater increase in their autofluorescence. Another clear influence of vitamin A was seen when +E, +A retinas autofluoresced not only much more than +E, -A retinas, which had similar numbers of granules, but also more than -E, -A retinas, which had about twice as many lipofuscin granules. In the retina, unlike the uterus, the lipofuscin-specific autofluorescence and lipofuscin granule number were not proportional. Moreover, the numbers of granules were influenced by both vitamins E and A, whereas the intensity of lipofuscin-specific autofluorescence was determined almost exclusively by vitamin A. Probably the accelerated loss of photoreceptor cells in -E, -A retinas resulted from both oxidation of membranes and oxidation of retinal vitamin A stores in the absence of vitamin E protection.