Murty V L, Piotrowski J, Morita M, Slomiany A, Slomiany B L
Research Center, New Jersey Dental School, University of Medicine and Dentistry, Newark 07103-2400.
Biochem Int. 1992 May;26(6):1091-9.
A glycosulfatase activity toward gastric sulfomucin was identified in the extracellular material elaborated by H. pylori. The enzyme exhibited maximum activity at pH 5.7 in the presence of Triton X-100 and CaCl2, and displayed on SDS-PAGE an apparent molecular weight of 30kDa. The H. pylori glycosulfatase effectively caused desulfation of N-acetylglucosamine-6-sulfate and galactose-6-sulfate of the carbohydrate chains of mucins, as well as that of glucose-6-sulfate of glyceroglucolipids, but was ineffective towards galactosyl- and lactosylceramide sulfates which contain galactose-3-sulfate. The glycosulfatase activity towards human gastric sulfomucin was affected by an antiulcer agent, nitecapone, which at its optimal concentration (100 micrograms/ml) caused a 61% inhibition. The results show that H. pylori through its glycosulfatase activity causes desulfation of sulfated mucins and glyceroglucolipids of the protective mucus layer, and that nitecapone is able to interfere with this detrimental action.
在幽门螺杆菌分泌的细胞外物质中鉴定出一种针对胃硫酸粘蛋白的糖硫酸酯酶活性。该酶在含有Triton X-100和CaCl2的条件下，于pH 5.7时表现出最大活性，在SDS-PAGE上显示的表观分子量为30kDa。幽门螺杆菌糖硫酸酯酶可有效使粘蛋白糖链中的N-乙酰葡糖胺-6-硫酸酯和半乳糖-6-硫酸酯以及甘油葡糖脂的葡萄糖-6-硫酸酯脱硫，但对含有半乳糖-3-硫酸酯的半乳糖基和乳糖基神经酰胺硫酸盐无效。针对人胃硫酸粘蛋白的糖硫酸酯酶活性受到抗溃疡药物硝替卡朋的影响，在其最佳浓度（100微克/毫升）下可导致61%的抑制率。结果表明，幽门螺杆菌通过其糖硫酸酯酶活性导致保护性粘液层的硫酸化粘蛋白和甘油葡糖脂脱硫，并且硝替卡朋能够干扰这种有害作用。
