Helicobacter pylori cagA Gene Polymorphism Affects the Total Antioxidant Capacity of Human Saliva Maciej Wnuk, * Aleksander Myszka, * Anna Lewinska, † Iwona Tokarz, * Katarzyna Solarska † and Grzegorz Bartosz †,‡ * Department of Genetics, University of Rzeszow, Rzeszow, Poland, † Department of Biochemistry and Cell Biology, University of Rzeszow, Rzeszow, Poland, ‡ Department of Molecular Biophysics, University of Lodz, Lodz, Poland Introduction Helicobacter pylori, a Gram-negative bacterium colonizing the human gastric mucosa of about 50% of the world population, is classified as a class I carcinogen [1] and is thought to be an important risk factor for chronic gastritis, peptic ulcer and gastric cancer [2–4]. Never- theless, mechanisms underlying H. pylori involvement in the pathogenesis of human gastric diseases, especially the host-pathogen interactions, are still poorly under- stood. The clinical manifestation of the disease may depend on many factors, including H. pylori genotype, innate host physiology, genetic predisposition and envi- ronmental factors [5]. H. pylori synthesizes a numerous of virulence factors like urease, arginase, adhesin (BabA), vacuolating toxin (VacA) or cytotoxin-associated antigen (CagA). Essen- tially, the virulence is linked to the occurrence of H. pylori genomic fragment with 29 genes, like cagA, E, G, H, I, L or M, namely the cag gene pathogenicity island required for proinflammatory response of gastric epithe- lial cells [5,6]. Oxidative stress plays an important role in the patho- genesis of H. pylori-mediated gastric disorders [7–13]. It was shown that infection with cagA+ H. pylori strains was correlated with a massive increase in oxidative DNA damage of host cells compared to cagA- H. pylori infection [14]. Moreover, cagA gene was found impor- tant to maintain antioxidative defense of H. pylori since knock-out of cagA gene was responsible for downregu- lation of superoxide dismutase or alkyl hydroperoxide reductase which may be a novel mechanism implicated in H. pylori pathogenesis [15]. Additionally, the level of reduced glutathione (GSH) was significantly lower in H. pylori-infected patients than in H. pylori-free subjects [16], which in turn may be associated with gastric carcinogenesis [17]. Therefore, the protective effects of various antioxidants (like vitamin E, vitamin C or Keywords cagA gene, Helicobacter pylori, saliva, total antioxidant capacity. Reprint requests to: Maciej Wnuk, Department of Genetics, University of Rzeszow, Rejtana 16C, PL 35-959, Rzeszow, Poland. Tel.: +48178723704, Fax.: +48178723708, E- mail: mawnuk@gmail.com Abstract Background: We aimed to evaluate the total antioxidant capacity (TAC) of saliva in healthy Helicobacter pylori-positive and negative saliva individuals. Materials and Methods: A total of 102 human saliva samples were checked for the presence of H. pylori DNA (ureA and cagA gene fragments). TAC of saliva was estimated by ABTS radical cation (ABTS •+ ) decoloriza- tion assay. Results: PCR analysis revealed that 36 subjects were ureA- ⁄ cagA-, 24 were ureA+ ⁄ cagA- and 42 were ureA+ ⁄ cagA+. Smoking habits had no evident effect on H. pylori infection. We found that TAC of the ureA- ⁄ cagA- material, after 10 seconds reaction reflecting fast-reacting antioxidants, was significantly higher than of ureA+ ⁄ - cagA- and ureA+ ⁄ cagA+ samples (p < .01 and p < .001, respectively). Similar results were obtained for reaction time of 3 minutes measuring slow-reacting antioxidants (p < .001). We also estimated ureA+ ⁄ cagA- and ureA+ ⁄ cagA+ samples alone and reported a statistically significant decrease in the TAC 3min value of ureA+ ⁄ cagA+ compared with ureA+ ⁄ cagA- samples (p < .05). Conclusions: Our data demonstrated that altered redox equilibrium may be associated with more frequent occurrence of H. pylori in the saliva samples. Helicobacter ISSN 1523-5378 ª 2010 Blackwell Publishing Ltd, Helicobacter 15: 53–57 53