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糖尿病性和半乳糖血症性白内障。

Diabetic and galactosaemic cataracts.

作者信息

Kador P F, Kinoshita J H

出版信息

Ciba Found Symp. 1984;106:110-31. doi: 10.1002/9780470720875.ch7.

Abstract

An increased prevalence of cataract is associated with diabetes. Biochemical studies of diabetic lenses have revealed a variety of metabolic abnormalities including changes in the levels of electrolytes, glutathione, nucleotides and sugars. Similar biochemical changes have also been observed in cataracts associated with galactosaemia, suggesting that these sugar cataracts have a common biochemical aetiology. The common biochemical factor found to initiate both types of sugar cataract is the formation of sugar alcohols (polyols) from either glucose or galactose by the enzyme aldose reductase (alditol: NADP+ 1-oxidoreductase, EC 1.1.1.21). Increased intracellular levels of these polar alcohols have a hyperosmotic effect which leads to lens fibre swelling, vacuole formation and subsequent opacification. The process of sugar cataract formation in animals can be prevented by inhibiting aldose reductase.

摘要

白内障患病率的增加与糖尿病相关。对糖尿病晶状体的生化研究揭示了多种代谢异常,包括电解质、谷胱甘肽、核苷酸和糖类水平的变化。在与半乳糖血症相关的白内障中也观察到了类似的生化变化,这表明这些糖性白内障具有共同的生化病因。发现引发这两种糖性白内障的共同生化因素是通过醛糖还原酶(醛糖醇:NADP+ 1-氧化还原酶,EC 1.1.1.21)将葡萄糖或半乳糖转化为糖醇(多元醇)。这些极性醇细胞内水平的升高具有高渗作用,导致晶状体纤维肿胀、液泡形成及随后的混浊。通过抑制醛糖还原酶可预防动物体内糖性白内障的形成过程。

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