Diabetic and galactosaemic cataracts.

Diabetic and galactosaemic cataracts.
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糖尿病和半乳糖血症性白内障。

DOI:
--
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发表时间:
1984
期刊:
Ciba Foundation symposium
影响因子:
--
通讯作者:
J. Kinoshita
J. Kinoshita
中科院分区:
--
文献类型:
--
作者:
P. Kador;J. Kinoshita

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白内障患病率的增加与糖尿病有关。糖尿病晶状体的生化研究揭示了各种代谢异常,包括电解质、谷胱甘肽、核苷酸和糖水平的变化。在与半乳糖血症相关的白内障中也观察到类似的生化变化,表明这些糖性白内障具有共同的生化病因。发现引发两种类型的糖性白内障的共同生物化学因素是通过酶醛糖还原酶(alditol:NADP+ 1-氧化还原酶,EC 1.1.1.21)由葡萄糖或半乳糖形成糖醇(多元醇)。这些极性醇的细胞内水平增加具有高渗效应,其导致透镜纤维肿胀、空泡形成和随后的混浊。动物糖性白内障形成过程可以通过抑制醛糖还原酶来预防。
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.
糖基化在蛋白质二硫键形成和白内障发生中的作用。
DOI: 10.1016/0014-4835(80)90086-x
发表时间: 1980
影响因子: 3.4
作者:
Ansari,NH;Awasthi,YC;Srivastava,SK
通讯作者: Srivastava,SK
甘油醛和其他简单单糖对氧合血红蛋白的氧化。
DOI: 10.1042/bj2170615
发表时间: 1984
期刊: The Biochemical journal
影响因子: --
作者:
Thornalley,PJ;Wolff,SP;Crabbe,MJ;Stern,A
通讯作者: Stern,A
单个完整兔晶状体中糖性白内障发生的 13C 核磁共振研究。
DOI: --
发表时间: 1982
影响因子: 4.4
作者:
Gonzalez,RG;Willis,J;Aguayo,J;Campbell,P;ChylackJr,LT;Schleich,T
通讯作者: Schleich,T