Organisciak D T, Wang H M, Noell W K, Plantner J J, Kean E L
Exp Eye Res. 1986 Jan;42(1):73-82. doi: 10.1016/0014-4835(86)90018-7.
Weanling albino rats were fed a vitamin-A-adequate diet or vitamin-A-deficient diet and maintained in a cyclic light or dark environment for up to 14 weeks. One half of the rats were supplemented with additional dietary linolenic acid in the form of linseed oil. The lipid composition and rhodopsin-opsin contents of isolated rod outer segments were determined after 6-7 weeks or 12-14 weeks on diet. This study shows that feeding rats a standard vitamin A-adequate or -deficient diet results in an age-dependent loss of omega three docosahexaenoic acid and a concomitant increase in omega six docosapentanoic acid in the rod outer segments. The loss of docosahexaenoate appears to be caused by insufficient dietary omega three fatty acids. The increase in omega six docosapentanoic acid appears to arise from the high concentration of linoleic acid in standard diets containing either cottonseed, or peanut oil or supplemental corn oil. Feeding rats diets supplemented with linseed oil, however, results in a rod outer-segment lipid profile which is the same as for chow-fed animals. The same effects were seen in the fatty-acid profile of lipids from liver, although the content of polyunsaturates was much lower than in rod outer segments. Vitamin A deficiency, itself, does not lead to changes in the fatty-acid composition of either the rod outer segments or liver. After 6-7 weeks on A+ or A- diet, rhodopsin levels were, as expected, higher in dark-reared rats than in cyclic-light animals. Although the rhodopsin levels in dark-reared vitamin A-adequate rats were significantly higher than in vitamin A-deficient animals, measurements of the lipid to opsin ratio of rod outer segments indicate that the rods of vitamin A-deficient rats are not markedly different than those of vitamin A-adequate rats. It is concluded that these diets may be useful in providing a means for evaluating the role of docosahexaenoic acid in visual cell death from damaging light.
将断乳的白化大鼠喂以维生素A充足或缺乏的饮食,并在循环光照或黑暗环境中饲养长达14周。一半的大鼠以亚麻籽油的形式补充额外的膳食亚麻酸。在饮食6 - 7周或12 - 14周后,测定分离的视杆细胞外段的脂质组成和视紫红质 - 视蛋白含量。本研究表明,给大鼠喂食标准的维生素A充足或缺乏的饮食会导致视杆细胞外段中ω-3二十二碳六烯酸随年龄增长而流失,同时ω-6二十二碳五烯酸相应增加。二十二碳六烯酸的流失似乎是由于膳食中ω-3脂肪酸不足所致。ω-6二十二碳五烯酸的增加似乎源于含有棉籽油、花生油或补充玉米油的标准饮食中亚油酸的高浓度。然而,给大鼠喂食补充亚麻籽油的饮食会导致视杆细胞外段脂质谱与喂食普通食物的动物相同。在肝脏脂质的脂肪酸谱中也观察到了相同的效果,尽管多不饱和脂肪酸的含量远低于视杆细胞外段。维生素A缺乏本身不会导致视杆细胞外段或肝脏的脂肪酸组成发生变化。在A +或A -饮食6 - 7周后,如预期的那样,黑暗饲养的大鼠视紫红质水平高于循环光照的动物。尽管黑暗饲养的维生素A充足大鼠的视紫红质水平显著高于维生素A缺乏动物,但对视杆细胞外段脂质与视蛋白比率的测量表明,维生素A缺乏大鼠的视杆细胞与维生素A充足大鼠的视杆细胞没有明显差异。得出的结论是,这些饮食可能有助于提供一种手段来评估二十二碳六烯酸在因有害光线导致的视觉细胞死亡中的作用。