Beil W, Birkholz C, Wagner S, Sewing K F
Department of General Pharmacology, Medizinische Hochschule Hannover, Germany.
Pharmacology. 1995 May;50(5):333-7. doi: 10.1159/000139299.
The effects of various types of antiulcer agents against Helicobacter pylori F1-ATPase were studied. ATPase was released into the aqueous phase (i.e., solubilized) by sonication. The enzyme activity depended on Mg2+, but not Ca2+. The maximum activity occurred at an ATP/Mg2+ ratio of 1/5 and at pH 7.5. Mg(2+)-dependent ATPase activity was inhibited by sodium azide and the monovalent cations K+ and Na+, but not by oligomycin, dicyclohexylcarbodiimide, ouabain, or SCH 28080. The antiulcer agents ranitidine, pirenzepine, aluminum hydroxide, and sucralfate failed to influence H. pylori F1-ATPase. In contrast, bismuth subcitrate and the H+/K(+)-ATPase inhibitor omeprazole inhibited the enzyme. Inhibition was prevented and reversed by the mercaptan glutathione, indicating that both drugs interfere with sulfhydryl groups of the enzyme. The data suggest that bismuth subcitrate and omeprazole owe their antibacterial activity against H. pylori, at least in part, to inhibition of F1-ATPase, an enzyme involved in bacterial energy metabolism.
研究了各类抗溃疡药物对幽门螺杆菌F1 - ATP酶的作用。通过超声处理将ATP酶释放到水相（即溶解）中。该酶的活性依赖于Mg2 +，而非Ca2 +。最大活性出现在ATP/Mg2 +比例为1/5且pH值为7.5时。Mg(2 +)依赖的ATP酶活性受到叠氮化钠以及单价阳离子K +和Na +的抑制，但不受寡霉素、二环己基碳二亚胺、哇巴因或SCH 28080的抑制。抗溃疡药物雷尼替丁、哌仑西平、氢氧化铝和硫糖铝未能影响幽门螺杆菌F1 - ATP酶。相反，枸橼酸铋和H +/K( +)-ATP酶抑制剂奥美拉唑抑制了该酶。巯基谷胱甘肽可防止并逆转这种抑制作用，表明这两种药物均干扰了该酶的巯基。数据表明，枸橼酸铋和奥美拉唑对幽门螺杆菌的抗菌活性至少部分归因于对F1 - ATP酶的抑制，该酶参与细菌能量代谢。
