Sadowska-Bartosz Izabela, Stefaniuk Ireneusz, Galiniak Sabina, Bartosz Grzegorz
Department of Biochemistry and Cell Biology, Faculty of Biology and Agriculture, University of Rzeszów, Rzeszów, Poland.
Teaching and Research Center of Microelectronics and Nanotechnology, Faculty of Mathematics and Natural Sciences, University of Rzeszów, Poland.
Redox Biol. 2015 Dec;6:93-99. doi: 10.1016/j.redox.2015.06.017. Epub 2015 Jul 2.
Ascorbic acid (AA) has been reported to be both pro-and antiglycating agent. In vitro, mainly proglycating effects of AA have been observed. We studied the glycation of bovine serum albumin (BSA) induced by AA in vitro. BSA glycation was accompanied by oxidative modifications, in agreement with the idea of glycoxidation. Glycation was inhibited by antioxidants including polyphenols and accelerated by 2,2'-azobis-2-methyl-propanimidamide and superoxide dismutase. Nitroxides, known to oxidize AA, did not inhibit BSA glycation. A good correlation was observed between the steady-state level of the ascorbyl radical in BSA samples incubated with AA and additives and the extent of glycation. On this basis we propose that ascorbyl radical, in addition to further products of AA oxidation, may initiate protein glycation.
据报道，抗坏血酸（AA）既是促糖化剂又是抗糖化剂。在体外，主要观察到AA的促糖化作用。我们研究了AA在体外诱导的牛血清白蛋白（BSA）糖基化。BSA糖基化伴随着氧化修饰，这与糖氧化的概念一致。糖基化受到包括多酚在内的抗氧化剂的抑制，并被2,2'-偶氮双-2-甲基丙脒和超氧化物歧化酶加速。已知能氧化AA的氮氧化物并不抑制BSA糖基化。在与AA和添加剂一起孵育的BSA样品中，抗坏血酸自由基的稳态水平与糖基化程度之间观察到良好的相关性。在此基础上，我们提出，除了AA氧化的进一步产物外，抗坏血酸自由基可能引发蛋白质糖基化。
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