OXIDATIVE GLYCATION AND FREE-RADICAL PRODUCTION - A CAUSAL MECHANISM OF DIABETIC COMPLICATIONS

被引:155
作者
HUNT, JV
WOLFF, SP
机构
[1] Department of Clinical Pharmacology, University College London, London WCI 655
来源
FREE RADICAL RESEARCH COMMUNICATIONS | 1991年 / 12-3卷
基金
英国医学研究理事会;
关键词
GLUCOSE OXIDATION; PROTEIN MODIFICATION; FREE RADICALS;
D O I
10.3109/10715769109145775
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Glucose may oxidise under physiological conditions and lead to the production of protein reactive ketoaldehydes, hydrogen peroxide and highly reactive oxidants. Glucose is thus able to modify proteins by the attachment of its oxidation derived aldehydes, leading to the development of novel protein fluoro-phores, as well as fragment protein via free radical mechanisms. The fragmentation of protein by glucose is inhibitable by metal chelators such as diethylenetriamine pentaacetic acid (DETAPAC) and free radical scavengers such as benzoic acid, and sorbitol. The enzymic antioxidant, catalase, also inhibits protein fragmentation. Protein glycation and protein oxidation are inextricably linked. Indeed, using boronate affinity chromatography to separate glycated from non-glycated material, we demonstrate that proteins which arc glycated exhibit an enhanced tryptophan oxidation. Our observation that both glycation and oxidation occur simultaneously further supports the hypothesis that tissue damage associated with diabetes and ageing has an oxidative origin. © 1991 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.
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页码:115 / 123
页数:9
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