Dong J W, Shi A Y
Department of Pathophysiology, Beijing Medical University.
Sheng Li Xue Bao. 1997 Dec;49(6):644-8.
Short term hypoxia induced endothelial cells (ECs) injury, as manifested in increasing lactate dehydrogenase (LDH) release and malondialdehyde (MDA) content, decreasing nitric oxide (NO) production and antioxidant enzyme glutathione peroxidase (GSH-Px) activity and increased intracellular calcium concentration, which were further exaggerated by reoxygenation. Administration of 200 U/ml superoxide dismutase (SOD) before hypoxia could partially prevent EC from such injuries, suggesting that the presence of oxygen free radicals may be one of the main factors involved in hypoxia-reoxygenation injury. The ameliorative effect of SOD in case is obviously due to elimination of oxygen free radicals.
短期缺氧可诱导内皮细胞（ECs）损伤，表现为乳酸脱氢酶（LDH）释放增加、丙二醛（MDA）含量增加、一氧化氮（NO）生成减少、抗氧化酶谷胱甘肽过氧化物酶（GSH-Px）活性降低以及细胞内钙浓度升高，而复氧会使这些损伤进一步加剧。在缺氧前给予200 U/ml超氧化物歧化酶（SOD）可部分预防内皮细胞遭受此类损伤，这表明氧自由基的存在可能是参与缺氧-复氧损伤的主要因素之一。本病例中SOD的改善作用明显归因于氧自由基的清除。
