Davidge S T, Ojimba J, McLaughlin M K
Perinatal Research Centre, Department of Obstetrics/Gynaecology, University of Alberta, Edmonton, Canada.
Hypertension. 1998 Mar;31(3):830-5. doi: 10.1161/01.hyp.31.3.830.
We tested the hypothesis that oxidative stress, mediated by dietary vitamin E deprivation, would alter vascular function through the interaction of oxygen-derived free radicals and nitric oxide (NO). This interaction may play an important role in the vascular pathophysiology of many diseases associated with oxidative stress. Mesenteric arteries from control (n = 12) and vitamin E-deprived (n = 12) Sprague-Dawley rats were studied with a myograph. Superoxide dismutase, which scavenges superoxide anions, produced a significantly greater relaxation in the arteries from the vitamin E-deprived rats compared with the controls (P<.05). Superoxide dismutase and catalase produced results similar to superoxide dismutase alone. Pretreatment with an NO synthase inhibitor eliminated the superoxide dismutase-induced relaxation in arteries from both control and vitamin E-deprived rats. L-Arginine induced a greater relaxation in arteries of the vitamin E-deprived group (P<.05). Agonist-induced relaxation with methacholine was not altered by superoxide dismutase for either group of animals, indicating that stimulated release of NO was not influenced by superoxide anions. With the use of Western immunoblot analysis, nitrotyrosine residues were shown to be present in arteries from both the vitamin E-deprived and control rats, but the amount of nitrotyrosine observed was not different between the two groups. In summary, our data indicate that there is a greater inhibition of NO caused by superoxide anions in the vitamin E-deprived group. We speculate that in conditions of oxidative stress (reduced vitamin E levels), altered vascular function may be due to increased destruction of NO by oxygen-derived free radicals.
饮食中缺乏维生素E介导的氧化应激会通过氧衍生自由基与一氧化氮（NO）的相互作用改变血管功能。这种相互作用可能在许多与氧化应激相关疾病的血管病理生理学中起重要作用。使用肌张力测定仪研究了对照（n = 12）和缺乏维生素E（n = 12）的Sprague-Dawley大鼠的肠系膜动脉。超氧化物歧化酶可清除超氧阴离子，与对照组相比，在缺乏维生素E的大鼠的动脉中，超氧化物歧化酶产生了显著更大的舒张作用（P<0.05）。超氧化物歧化酶和过氧化氢酶产生的结果与单独使用超氧化物歧化酶时相似。用一氧化氮合酶抑制剂预处理可消除超氧化物歧化酶诱导的对照大鼠和缺乏维生素E的大鼠动脉的舒张作用。L-精氨酸在缺乏维生素E的组的动脉中诱导了更大的舒张作用（P<0.05）。两组动物中，超氧化物歧化酶均未改变乙酰甲胆碱引起的激动剂诱导的舒张作用，这表明超氧阴离子不影响一氧化氮的刺激释放。通过蛋白质免疫印迹分析，发现缺乏维生素E的大鼠和对照大鼠的动脉中均存在硝基酪氨酸残基，但两组中观察到的硝基酪氨酸数量没有差异。总之，我们的数据表明，在缺乏维生素E的组中，超氧阴离子对一氧化氮的抑制作用更大。我们推测，在氧化应激（维生素E水平降低）的情况下，血管功能改变可能是由于氧衍生自由基对一氧化氮的破坏增加所致。
