Suttorp N, Toepfer W, Roka L
Am J Physiol. 1986 Nov;251(5 Pt 1):C671-80. doi: 10.1152/ajpcell.1986.251.5.C671.
The importance of the glutathione (GSH) redox cycle and of catalase as intracellular antioxidant defense systems in cultured endothelial cells against an extracellular flux of H2O2, a critical mediator of polymorphonuclear leukocyte-induced oxidant injury of endothelial cells, was examined. The activities of different parts of the GSH redox cycle were impaired by 1,3-bis(2-chloroethyl)-1-nitrosourea, buthionine sulfoximine, diethyl maleate and 2-cyclohexene-1-one. Catalase activity was inhibited by 3-amino-1,2,4-triazole. After an impairment of the GSH redox cycle, but not of catalase, the susceptibility of pulmonary artery endothelial cells to an attack by H2O2 was dramatically increased independent of the source of extracellularly generated hydrogen peroxide (i.e., glucose oxidase or stimulated polymorphonuclear leukocytes). Exogenous catalase, d-alpha-tocopherol, and particularly Trolox, the chroman compound of tocopherol, but not phytol, the fatty acid side chain of tocopherol, provided almost complete protection of the endothelial cells against a H2O2-mediated attack. Additional fluorometric studies suggested that H2O2 is scavenged by the antioxidants before it hits the target cells.
研究了谷胱甘肽（GSH）氧化还原循环和过氧化氢酶作为培养的内皮细胞内抗氧化防御系统，抵御细胞外过氧化氢通量的重要性，过氧化氢是多形核白细胞诱导的内皮细胞氧化损伤的关键介质。GSH氧化还原循环不同部分的活性受到1,3-双（2-氯乙基）-1-亚硝基脲、丁硫氨酸亚砜胺、马来酸二乙酯和2-环己烯-1-酮的损害。过氧化氢酶活性受到3-氨基-1,2,4-三唑的抑制。在GSH氧化还原循环受损后，而非过氧化氢酶受损后，肺动脉内皮细胞对过氧化氢攻击的敏感性显著增加，且与细胞外产生过氧化氢的来源（即葡萄糖氧化酶或刺激的多形核白细胞）无关。外源性过氧化氢酶、d-α-生育酚，尤其是生育酚的苯并二氢吡喃化合物Trolox，而非生育酚的脂肪酸侧链植醇，几乎能完全保护内皮细胞免受过氧化氢介导的攻击。额外的荧光研究表明，过氧化氢在攻击靶细胞之前就被抗氧化剂清除了。
