Endotoxin increases superoxide dismutase in cultured bovine pulmonary endothelial cells.
Endotoxin increases superoxide dismutase in cultured bovine pulmonary endothelial cells.
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内毒素会增加培养的牛肺内皮细胞中的超氧化物歧化酶。
DOI：
10.1152/ajpcell.1987.252.4.c436
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Burr,IM
中科院分区：
文献类型：
--
作者：
Shiki,Y;Meyrick,BO;Brigham,KL;Burr,IM
在接触和不接触大肠杆菌内毒素（10(-1) µg/ml）的培养牛肺内皮细胞中，以0.5-24小时的间隔测量锰（Mn）和铜锌（CuZn）超氧化物歧化酶（SOD）浓度以及谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）活性。还测量了两种线粒体标记酶延胡索酸酶和细胞色素c氧化酶的活性。内毒素暴露导致内皮细胞 Mn SOD 含量显着增加（9 倍），但对 GSH-Px、CAT、延胡索酸酶或细胞色素 C 氧化酶活性没有显着影响。内毒素导致 CuZn SOD 含量在 24 小时内略有下降。这是内毒素对肺内皮细胞中 Mn SOD 选择性作用的首次报道。该反应似乎与线粒体活性的增加无关（未观察到细胞色素 C 氧化酶或延胡索酶活性的变化）。这些发现支持内毒素增加肺内皮细胞内有毒氧代谢物的产生的观点。内毒素诱导的 Mn SOD 增加可能有助于内毒素对这些细胞中氧毒性的保护作用。
Manganous (Mn) and copper zinc (CuZn) superoxide dismutase (SOD) concentrations and glutathione peroxidase (GSH-Px) and catalase (CAT) activities were measured in cultured bovine pulmonary endothelial cells with and without exposure to Escherichia coli endotoxin (10(-1) micrograms/ml) over intervals of 0.5-24 h. The activities of two mitochondrial marker enzymes, fumarase and cytochrome-c oxidase, were also measured. Endotoxin exposure caused a marked increase (9-fold) in endothelial cell Mn SOD content without significant effects on GSH-Px, CAT, fumarase, or cytochrome-c oxidase activities. Endotoxin induced a slight decrease in CuZn SOD content over 24 h. This is the first report of a selective effect of endotoxin on Mn SOD in pulmonary endothelial cells. The response appears to be independent of an increase in mitochondrial activity (no change was observed in cytochrome-c oxidase or fumarase activities). These findings support the notion that endotoxin increases generation of toxic oxygen metabolites within pulmonary endothelial cells. An endotoxin-induced increase in Mn SOD could contribute to the reported protective effect of endotoxin against oxygen toxicity in these cells.