title: Inhibitory actions of luteolin on the growth and arylamine N-acetyltransferase activity in strains of Helicobacter pylori from ulcer patients.
abstract: Helicobacter pylori is now recognized as an important cause of type B gastritis, which is strongly associated with gastric and duodenal ulcer disease. H. pylori may be a causative factor in patients with gastric cancer. The growth inhibition and N-acetylation of 2-Aminofluorene (AF) or P-aminobenzoic acid (PABA) by arylamine N-acetyltransferase (NAT) in H. pylori were inhibited by luteolin, a component in herbal medicine. The growth inhibition was based on the changes of optical density (OD) by using a spectrophotometer. The N-acetylation of AF or PABA by NAT from H. pylori were assayed by the amounts of acetylated and non-acetylated AF or PABA in cytosols and intact bacteria of H. pylori by using HPLC. An inhibition of growth on H. pylori demonstrated that luteolin elicited a dose-dependent growth inhibition in the H. pylori cultures. Cytosols and suspensions of H. pylori with or without specific concentrations of luteolin co-treatment showed different percentages of AF or PABA acetylation. The data indicated that there was decreased NAT activity associated with increased levels of luteolin in H. pylori cytosols and suspensions. Using standard steady-state kinetic analysis, it was demonstrated that luteolin was a possible uncompetitive inhibitor to NAT enzyme in H. pylori. This report is the first demonstration to show that luteolin can inhibit H. pylori growth and NAT activity.
authors.affiliation: Department of Microbiology, China Medical College, 400, ROC, 91 Szueh-Shih Road, Taichung, Taiwan. jgchung@mailcmc.edu.tw
authors.forename: J G
authors.initials: JG
authors.lastname: Chung
authors.forename: T C
authors.initials: TC
authors.lastname: Hsia
authors.forename: H M
authors.initials: HM
authors.lastname: Kuo
authors.forename: Y C
authors.initials: YC
authors.lastname: Li
authors.forename: Y M
authors.initials: YM
authors.lastname: Lee
authors.forename: S S
authors.initials: SS
authors.lastname: Lin
authors.forename: C F
authors.initials: CF
authors.lastname: Hung
mesh_terms: D010129:4-Aminobenzoic Acid / Q000378:metabolism; D000107:Acetylation / Q000187:drug effects; D001191:Arylamine N-Acetyltransferase / Q000378:metabolism*; D002470:Cell Survival; D002851:Chromatography, High Pressure Liquid; D003600:Cytosol / Q000187:drug effects / Q000201:enzymology*; D004305:Dose-Response Relationship, Drug; D005419:Flavonoids / Q000494:pharmacology*; D005449:Fluorenes / Q000378:metabolism / Q000493:pharmacokinetics; D005756:Gastritis / Q000382:microbiology; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000187:drug effects* / Q000201:enzymology* / Q000254:growth & development; D006801:Humans; D007700:Kinetics; D047311:Luteolin; D008826:Microbial Sensitivity Tests; D010437:Peptic Ulcer / Q000382:microbiology*; D012680:Sensitivity and Specificity; D013997:Time Factors
chemical_list: D005419:Flavonoids; D005449:Fluorenes; D001191:Arylamine N-Acetyltransferase; D047311:Luteolin; D010129:4-Aminobenzoic Acid