高血糖环境中的晚期糖基化终产物和氧化应激

A. Nakamura, Ritsuko Kawahrada
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引用次数: 4

摘要

蛋白质糖基化是糖尿病和衰老诱导的糖与蛋白质的随机、非酶反应;这个过程与糖基转移酶催化的酶促反应介导的糖基化有很大的不同。希夫碱通过中间体形成晚期糖基化终产物(AGEs),如Amadori化合物。虽然这些AGEs形成了各种各样的分子种类,但它们的结构只有少数被确定。AGEs与细胞膜上不同的AGE受体结合并向细胞传递信号。通过AGEs受体的信号转导在细胞中产生活性氧,氧化应激是糖尿病并发症的发病原因。本章介绍了高血糖环境下由蛋白糖基化产生的AGEs引起的氧化应激(包括活性氧)引起的疾病发病的分子机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Advanced Glycation End Products and Oxidative Stress in a Hyperglycaemic Environment
Protein glycation is the random, nonenzymatic reaction of sugar and protein induced by diabetes and ageing; this process is quite different from glycosylation mediated by the enzymatic reactions catalysed by glycosyltransferases. Schiff bases form advanced glycation end products (AGEs) via intermediates, such as Amadori compounds. Although these AGEs form various molecular species, only a few of their structures have been determined. AGEs bind to different AGE receptors on the cell membrane and transmit signals to the cell. Signal transduction via the receptor of AGEs produces reactive oxygen species in cells, and oxidative stress is responsible for the onset of diabetic complications. This chapter introduces the molecular mechanisms of disease onset due to oxidative stress, including reactive oxygen species, caused by AGEs generated by protein glycation in a hyperglycaemic environment.
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