Arylamine N-acetyltransferase: a possible promoter in Helicobacter pylori-related gastric carcinogenesis.

ABSTRACT

BACKGROUND: The hypothesis of an association between peptic ulcer and infection by Helicobacter pylori in the gastroduodenal tract was suggested by Marshall and Warren in 1984. H pylori infection of the stomach is the most frequent infection in the world and exhibits an age-dependent increase. However, only a very small percentage of those infected develop gastric carcinoma, suggesting that H pylori acts as a cofactor in the pathogenesis of gastric carcinoma. N-Acetyltransferase (NAT) is expressed in uroepithelial cells and colon cytosol, while cytosolic acetyltransferase plays a critical role in susceptibility to arylamine-induced bladder and colon cancer. The presence of NAT activity in H pylori has yet to be determined. METHODS: NAT activity in H pylori from patients with peptic ulcer was studied using an acetyl coenzyme A (AcCoA) recycling assay and high-pressure liquid chromatography with p-aminobenzoic acid and aminofluorene substrates. RESULTS: The NAT activities from a number of H pylori samples were found to be 0.68 +/- 0.10 nmol/min/10(10) colony-forming units (CFUs) (intact bacteria); and 0.90 +/- 0.22 nmol/min/mg protein (cytosol) for the acetylation of 2-aminofluorene, and 0.63 +/- 0.06 nmol/min/10(10) CFUs (intact bacteria) and 0.72 +/- 0.24 nmol/min/mg protein (cytosol) for the acetylation of p-aminobenzoic acid. CONCLUSIONS: These studies show that H pylori has NAT activity, from which we speculate that the bioactivation of food-borne heterocyclic aromatic amines into genotoxic and carcinogenic products in the stomach is a possible promoter in the pathogenesis of gastric cancer.