Göttke M, Chadee K
Institute of Parasitology, Macdonald College, McGill University, St. Anne de Bellevue, Québec, Canada.
Inflamm Res. 1996 Apr;45(4):209-12. doi: 10.1007/BF02285163.
The effect of exogenous and endogenous nitric oxide on the secretion of mucins from the human colonic adenocarcinoma cell-line LS174T was studied. Mucin secretion was followed by measuring the release of [3H]-glucosamine metabolically labelled glycoproteins eluted in the void volume of Sepharose 4B column chromatography. In response to exogenously produced nitric oxide from sodium nitroprusside, mucin secretion occurred in a time- and dose-dependent fashion that preceded epithelial cell damage. However, in the presence of the nitric oxide scavenger myoglobin, mucin secretion and cell damage were abrogated. Endogenously produced nitric oxide did not affect mucin secretion as the addition of excess L-arginine, the substrate for nitric oxide synthase, the removal of arginine from the culture medium with arginase or the inhibition of nitric oxide synthase with the competitive inhibitor NG-monomethyl-L-arginine had no effect on basal mucin release. These results suggest that exogenously produced nitric oxide can directly affect mucin secretion as a cytoprotective mechanism.
研究了外源性和内源性一氧化氮对人结肠腺癌细胞系LS174T黏蛋白分泌的影响。通过测量在Sepharose 4B柱色谱空体积中洗脱的[3H]-葡萄糖胺代谢标记糖蛋白的释放来跟踪黏蛋白分泌。响应于硝普钠外源性产生的一氧化氮，黏蛋白分泌以时间和剂量依赖性方式发生，且先于上皮细胞损伤。然而，在一氧化氮清除剂肌红蛋白存在的情况下，黏蛋白分泌和细胞损伤被消除。内源性产生的一氧化氮不影响黏蛋白分泌，因为添加过量的一氧化氮合酶底物L-精氨酸、用精氨酸酶从培养基中去除精氨酸或用竞争性抑制剂NG-单甲基-L-精氨酸抑制一氧化氮合酶对基础黏蛋白释放均无影响。这些结果表明，外源性产生的一氧化氮可作为一种细胞保护机制直接影响黏蛋白分泌。
