Active oxygen-induced vascular damage and its protection.

1.膳食维生素E可减少由年龄增加（从3周龄至40周龄）引起的大鼠胸主动脉组胺诱导的内皮依赖性血管舒张和相关cGMP产生的减少。血浆过氧化脂质水平随年龄增加而增加，维生素E缺乏大鼠进一步增加，维生素E补充大鼠降低。维生素C和Fe ^<2 +>可在体外引发脂质过氧化反应，在E缺乏大鼠中，随着主动脉脂质过氧化反应的增加，组胺诱导的血管舒张和cGMP形成减少。补充维生素E可抑制脂质过氧化引起的血管舒张和cGMP合成的减少。这些结果表明，维生素E可能具有保护作用的减少血管舒张与年龄和体外脂质过氧化作用，由于其抗氧化活性。膳食维生素E对子宫输卵管结扎引起的胎儿缺血性窘迫有保护作用 ...更多信息 孕鼠脑缺血再灌注后，胎鼠脑组织脂质过氧化反应增强，SSELS可能通过抑制脂质过氧化反应而增强。补充维生素E可减轻大鼠脊髓缺血性压迫损伤引起的运动障碍，而缺乏维生素E则加重运动障碍。缺血后再灌注脊髓中脂质过氧化物水平的增加随着维生素E.3饮食水平的降低而增加。研究了胶束膜中螯合二铁催化H2O2依赖性、脂质过氧化物依赖性和非过氧化物依赖性脂质过氧化反应的位点特异性机制。在所检测的螯合剂如EDTA、EGTA、NH4PAC和去铁胺中，铁-NTA（次氮基三乙酸）（据报道其在肾脏中具有致癌作用）显示出最高的引发这三种脂质过氧化的活性，这表明铁-NTA的强促氧化作用是其肾脏致癌性的主要原因。少

1. Dietary vitamin E reduced the decreases of the histamin-induced, endothelium-dependent vasodilatation and associated production of cGMP in rat thoracic aorta induced by increase of age(from 3-weeks to 40-weeks). The level of plasma lipid peroxides increased with increase of age was further increased in vitamin E-deficient rats and decreased in vitamin E-supplemented rats. Histamin-induced vasodilatation and cGMP formation in E-deficient rats were decreased with increase of lipid peroxides in aorta by incubation with ascorbic acid and Fe^<2+>, which are known to initiate lipid peroxidation in vitro. The decreases of vasodilatation and cGMP synthesis by lipid peroxidation were suppressed in E-supplemented rats. These results indicate that vitamin E may have a protective effect on decrease -of vasodilatation associated with age and in vitro lipid peroxidation due to its antioxidant activity.2. Dietary vitamin E protected the fetal ischemic distress induced by clampig, the uterotubal ve … More ssels of pregnant rats, possibly by inhibiting lipid peroxidation increased in the fetal tissues such as brain by reperfusion after ischemia. Moter disturbances induced by ischemic compression injury of rat spinal cord were reduced by vitamin E-supplementation, but enhanced by vitamin E deficiency. The increase in the level of lipid peroxides in the spinal cord by reperfusion after ischemia increased with decrease in the dietary level of vitamin E.3. The site-specific mechanism of initiation of H202-dependent, lipid peroxidedependent and peroxide-independent lipid peroxidations catalyzed by chelatediron in micelle membranes was investigated. Among the chelaters examined such as EDTA, EGTA, DETAPAC, and deferoxamine, iron-NTA(nitrilotriacetic acid), which was reported to have carcinogenic effect in kidney, showed the highest activity for the initiation of these three lipid peroxidations, suggesting that the strong prooxidant effects of iron-NTA is a major cause of its renal carcinogenicity. Less