Antioxidant defense mechanisms of endothelial cells: glutathione redox cycle versus catalase.
Antioxidant defense mechanisms of endothelial cells: glutathione redox cycle versus catalase.
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内皮细胞的抗氧化防御机制：谷胱甘肽氧化还原循环与过氧化氢酶。
DOI：
10.1152/ajpcell.1986.251.5.c671
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
L. Róka
中科院分区：
文献类型：
--
作者：
N. Suttorp;W. Töpfer;L. Róka
谷胱甘肽（GSH）的氧化还原循环和过氧化氢酶作为细胞内的抗氧化防御系统在培养的内皮细胞对H2 O2，一个关键介质的多形核白细胞诱导的内皮细胞的氧化损伤的细胞外流量的重要性进行了检查。1，3-二（2-氯乙基）-1-亚硝基脲、丁硫基亚砜亚胺、马来酸二乙酯和2-环己烯-1-酮对GSH氧化还原循环不同部位的活性均有抑制作用。3-氨基-1，2，4-三唑对过氧化氢酶活性有抑制作用。在GSH氧化还原循环受损而非过氧化氢酶受损后，肺动脉内皮细胞对H2 O2攻击的敏感性显著增加，与细胞外产生的过氧化氢的来源无关（即，葡萄糖氧化酶或刺激的多形核白细胞）。外源性过氧化氢酶，d-α-生育酚，特别是Trolox，生育酚的色满化合物，但不是植醇，生育酚的脂肪酸侧链，提供了几乎完全的保护内皮细胞免受H2 O2介导的攻击。另外的荧光研究表明，H2 O2在击中靶细胞之前被抗氧化剂清除。
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.
DOI：
10.1016/s0021-9258(19)68180-9
发表时间：
1982-02
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
B. Arrick;C. Nathan;O. Griffith;Z. Cohn
通讯作者：
B. Arrick;C. Nathan;O. Griffith;Z. Cohn