Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.3.14 (ATP synthase)
 7,042 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Bismuth subcitrate and omeprazole inhibit Helicobacter pyloriF1-ATPase. 766 94