Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na++K+)-ATPase activity reduction in high glucose-treated human erythrocytes
Pyridoxine and pyridoxamine inhibits superoxide radicals and prevents lipid peroxidation, protein glycosylation, and (Na++K+)-ATPase activity reduction in high glucose-treated human erythrocytes
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DOI：
10.1016/s0891-5849(00)00462-7
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发表时间：
2001-02-01
影响因子：
7.4
通讯作者：
Lim, G
中科院分区：
文献类型：
--
作者：
Jain, SK;Lim, G
补充维生素B-6（吡哆醇）已被发现对预防糖尿病神经病变和视网膜病变以及蛋白质的糖基化有益。氧自由基和氧化损伤与糖尿病的细胞功能障碍和并发症有关。本研究旨在验证pyridoxine (P)和pyridoxamine （PM）在高糖暴露红细胞（RBC）中抑制超氧自由基产生、减少脂质过氧化和糖基化、增加(Na+ + K+)- atp酶活性的假说。通过在无细胞缓冲溶液中存在或不存在P或PM时葡萄糖对细胞色素C的还原来评估超氧自由基的产生。为了检验细胞效应，将洗净的正常人红细胞用对照和高葡萄糖浓度处理，加或不加P或PM。P和PM均可显著降低高葡萄糖暴露的RBC中脂质过氧化和糖化血红蛋白（HbA(1)）的形成。P和PM能显著抑制高糖处理红细胞(Na+ + K+)- atp酶活性的降低，从而抑制氧自由基的产生，从而抑制高血糖引起的脂质过氧化、蛋白糖基化和(Na+ + K+)- atp酶活性的降低。本研究描述了一种新的生化机制，通过补充P或PM可以延缓或抑制糖尿病并发症的发展。(C) 2001爱思唯尔科学公司
Vitamin B-6 (pyridoxine) supplementation has been found beneficial in preventing diabetic neuropathy and retinopathy, and the glycosylation of proteins. Oxygen radicals and oxidative damage have been implicated in the cellular dysfunction and complications of diabetes. This study was undertaken to test the hypothesis that pyridoxine (P) and pyridoxamine (PM) inhibit superoxide radical production, reduce lipid peroxidation and glycosylation, and increase the (Na+ + K+)-ATPase activity in high glucose-exposed red blood cells (RBC). Superoxide radical production was assessed by the reduction of cytochrome C by glucose in the presence and absence of P or PM in a cell-free buffered solution. To examine cellular effects, washed normal human RBC were treated with control and high glucose concentrations with and without P or PM. Both P and PM significantly lowered lipid peroxidation and glycated hemoglobin (HbA(1)) formation in high glucose-exposed RBC. P and PM significantly prevented the reduction in (Na+ + K+)- ATPase activity in high glucose-treated RBC, Thus, P or PM can inhibit oxygen radical production, which in turn prevents the lipid peroxidation, protein glycosylation, and (Na+ + K+)-ATPase activity reduction induced by the hyperglycemia. This study describes a new biochemical mechanism by which P or PM supplementation may delay or inhibit the development of complications in diabetes. (C) 2001 Elsevier Science Inc.