Oxidative stress:: the vulnerable β-cell
Oxidative stress:: the vulnerable β-cell
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DOI：
10.1042/bst0360343
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发表时间：
2008-06-01
影响因子：
3.9
通讯作者：
Lenzen, Sigurd
中科院分区：
文献类型：
--
作者：
Lenzen, Sigurd
胰腺β细胞的抗氧化防御机制特别弱，并且可能被由活性氧和活性氮物质的过度产生引起的氧化还原失衡所压倒。这种氧化还原失衡的后果是脂质过氧化、蛋白质氧化、DNA损伤和反应性物质干扰信号转导途径，这显著导致1型和2型糖尿病中的β细胞功能障碍和死亡。活性氧、超氧自由基（O-2（中心点-））、过氧化氢（H2 O2）以及在最终的铁催化反应步骤中最具反应性和毒性的羟基自由基（OH中心点）在1型糖尿病中的促炎性甜菜碱介导的β细胞攻击和2型糖尿病中的糖脂毒性介导的β细胞功能障碍期间产生。与本身有毒的NO中心点结合，以及通过其与O-2（中心点-）的反应和随后形成过氧亚硝酸盐，反应性物质在糖尿病发展中葡萄糖耐量恶化期间的β细胞死亡中起中心作用。
Antioxidative defence mechanisms of pancreatic beta-cells are particularly weak and can be overwhelmed by redox imbalance arising from overproduction of reactive oxygen and reactive nitrogen species. The consequences of this redox imbalance are lipid peroxidation, oxidation of proteins, DNA damage and interference of reactive species with signal transduction pathways, which contribute significantly to beta-cell dysfunction and death in Type 1 and Type 2 diabetes mellitus. Reactive oxygen species, superoxide radicals (O-2(center dot-)), hydrogen peroxide (H2O2) and, in a final iron-catalysed reaction step, the most reactive and toxic hydroxyl radicals (OH center dot) are produced during both pro-inflammatory cytokine-mediated beta-cell attack in Type 1 diabetes and glucolipotoxicity-mediated beta-cell dysfunction in Type 2 diabetes. in combination with NO center dot, which is toxic in itself, as well as through its reaction with the O-2(center dot-) and subsequent formation of peroxynitrite, reactive species play a central role in beta-cell death during the deterioration of glucose tolerance in the development of diabetes.