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糖性白内障中氧化还原状态异常但脂质过氧化未增加。

Abnormal redox status without increased lipid peroxidation in sugar cataract.

作者信息

Woollard A C, Bascal Z A, Armstrong G R, Wolff S P

机构信息

Department of Clinical Pharmacology, University College London, United Kingdom.

出版信息

Diabetes. 1990 Nov;39(11):1347-52. doi: 10.2337/diab.39.11.1347.

Abstract

In conflict with a previous report, we find that phenolic inhibitors of lipid peroxidation (butylated hydroxytoluene [BHT] and butylated hydroxyanisole [BHA]) do not have significant inhibitory effect on galactosemic cataract formation. This is consistent with the lack of enhancement of stable products of lipid peroxidation (measured by the thiobarbituric acid assay) in the lenses of galactosemic rats. This does not imply that oxidative stress plays no role in galactosemic cataract formation (indeed, we find that galactosemic lens homogenates contain increased amounts of an Fe2+ oxidant, possibly a peroxide), but rather that BHT- and BHA-inhibitable lipid peroxidation specifically has no role to play. In instances where drugs appear to inhibit galactosemic cataract formation, other effects caused by the drugs, e.g., inhibition of feeding or induction of general detoxification pathways, must be considered.

摘要

与之前的一份报告不同,我们发现脂质过氧化的酚类抑制剂(丁基羟基甲苯 [BHT] 和丁基羟基茴香醚 [BHA])对半乳糖血症性白内障的形成没有显著抑制作用。这与半乳糖血症大鼠晶状体中脂质过氧化稳定产物(通过硫代巴比妥酸测定法测量)缺乏增加是一致的。这并不意味着氧化应激在半乳糖血症性白内障形成中不起作用(事实上,我们发现半乳糖血症晶状体匀浆中Fe2+氧化剂的含量增加,可能是一种过氧化物),而是说BHT和BHA可抑制的脂质过氧化作用尤其不起作用。在药物似乎能抑制半乳糖血症性白内障形成的情况下,必须考虑药物引起的其他效应,例如抑制进食或诱导一般解毒途径。

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