Selenium, selenoproteins and vision
Selenium, selenoproteins and vision
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DOI：
10.1159/000082770
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发表时间：
2005-01-01
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影响因子：
--
通讯作者：
Flohé, L
中科院分区：
文献类型：
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作者：
Flohé, L
硒的生物化学方面进行审查，其推定的相关性与年龄有关的眼部疾病。硒是一种必需的微量元素，在哺乳动物体内至少有25种不同的硒酶中以硒代半胱氨酸残基的形式发挥其生理作用。由于食物硒缺乏导致的GPx-1缺乏已被推断为诱导大鼠白内障，并被证明通过靶向基因破坏导致小鼠白内障。其他硒蛋白在眼睛中的作用仍有待研究。硒蛋白合成所需的微量硒过量通常是有毒的，会导致实验动物的白内障。硒在白内障、黄斑变性、色素性视网膜炎或任何其他眼部疾病的发展中的保护作用的临床证据是不可用的，这可能是因为次优硒摄入量（可能由不平衡的饮食引起）不会引起眼睛中任何病理相关的硒缺乏。目前，在眼科疾病的背景下，除了55微克/天的膳食参考摄入量之外，还没有理论或经验基础来预期硒补充剂的有益作用。版权所有（c）2005 S. Karger AG，巴塞尔。
Selenium biochemistry is reviewed in respect to its presumed relevance to age-related ocular diseases. Selenium is an essential trace element that exerts its physiological role as selenocysteine residue in at least 25 distinct selenoenzymes in mammals. Lack of GPx-1 due to alimentary selenium deprivation has been inferred to induce cataract in rats and was demonstrated to cause cataracts in mice by targeted gene disruption. The role of other selenoproteins in the eye remains to be worked out. Selenium in excess of the tiny amounts required for selenoprotein synthesis is toxic in general and causes cataracts in experimental animals. Clinical evidence for a protective role of selenium in the development of cataract, macula degeneration, retinitis pigmentosa or any other ocular disease is not available, likely because suboptimum selenium intake, as it may result from unbalanced diet, does not cause any pathologically relevant selenium deficiency in the eye. At present, there is neither theoretical nor an empirical basis to expect beneficial effects of selenium supplementation beyond the dietary reference intakes of 55 mu g/day in the context of ocular diseases. Copyright (c) 2005 S. Karger AG, Basel.