Oxidative stress in the brain tissue of laboratory mice with acute post insulin hypoglycemia.
Oxidative stress in the brain tissue of laboratory mice with acute post insulin hypoglycemia.
复制标题
患有急性胰岛素后低血糖的实验小鼠脑组织中的氧化应激。
作者：
J. Patockova;P. Marhol;E. Tůmová;M. Kršiak;R. Rokyta;S. Stípek;J. Crkovská;M. Andel
丙二醛（MDA）、铜锌超氧化物歧化酶（Cu，Zn-SOD）和硒依赖的谷胱甘肽过氧化物酶（GSPHx）是目前认为的氧化应激的基本标志物。MDA是膜脂过氧化的终产物之一，而Cu、Zn-SOD和GSHPx则属于天然抗氧化剂。氧自由基在许多疾病的发病机制中的作用是有据可查的。本研究的目的是确定胰岛素诱导的急性低血糖对脑组织氧化应激的影响。通过腹腔内给予剂量为24 IU/kg的胰岛素，在ICR小鼠中诱导低血糖。MDA、Cu、Zn-SOD、GSHPx水平与低血糖严重程度相关。结果表明，在严重低血糖（血清葡萄糖浓度低于1.0 mmol/l）时，脑组织中的脂质过氧化（以MDA水平表示）高于正常血糖对照组（约3.7 mmol/l），也高于中度低血糖时的MDA水平（范围在1-2 mmol/l之间）。这表明在严重低血糖期间脑组织中的脂质过氧化作用增强。然而，这两种酶- Cu，Zn-SOD或GSHPx -没有表现出类似的趋势。
Malondialdehyde (MDA), Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and selenium-dependent glutathione peroxidase (GSPHx) are currently considered to be basic markers of oxidative stress. MDA is one of the end-products of the peroxidation of membrane lipids, whereas enzymes Cu,Zn-SOD and GSHPx belong to the natural antioxidants. The role of oxygen free radicals in the pathogenesis of many diseases is well documented. The aim of this study was to ascertain the influence of insulin-induced acute hypoglycemia on oxidative stress in the brain tissue. Hypoglycemia was induced in ICR mice by intraperitoneal administration of insulin at a dose 24 IU/kg. There was a correlation between the severity of hypoglycemia and the levels of MDA, Cu,Zn-SOD and GSHPx. The results showed that in severe hypoglycemia (serum glucose concentration below 1.0 mmol/l) the lipoperoxidation in brain tissue expressed as the level of MDA was higher in comparison with normoglycemic controls (glycemia around 3.7 mmol/l) as well as in comparison with the levels of MDA during moderate hypoglycemia (glycemia ranging between 1-2 mmol/l). This indicates the enhancement of lipoperoxidation in the brain tissue during severe hypoglycemia. However, both enzymes - Cu,Zn-SOD or GSHPx - did not show a similar tendency.