Helicobacter pylori gastritis affects gastric pH and concentrations of ascorbic acid, hydrogen peroxide, hypochlorite, ammonia and urea, pepsin, and mucin. First, the separate effects of each of these altered factors on oxidation of pork were investigated during in vitro gastrointestinal digestion. Lipid and protein oxidation increased (range 23-48%) in duodenal digests of pork previously exposed to elevated (6.1) versus normal acidic stomach pH (2.3 to 3.5) conditions. Salivary nitrite reduced the formation of lipid and protein oxidation products (range 14-20%) under normal acidic but not elevated stomach pH conditions. Higher amounts of hydrogen peroxide and lower amounts of ascorbic acid decreased concentrations of lipid oxidation products in duodenal pork digests, whereas ammonia slightly stimulated protein oxidation during digestion. Second, two H. pylori gastritis-duodenal digestion models were installed using a set of altered compound concentrations at normal acidic or elevated stomach pH. The elevated pH-gastritis-duodenal digestion model increased pork protein oxidation compared with the normal pH-gastritis and the normal digestion model (14.3 ± 2.1 vs 8.2 ± 1.0 nmol DNPH/mg protein, P < 0.001). Compared with the other models, protein oxidation was also increased when nitrite-cured pork was exposed to the elevated pH-gastritis-duodenal digestion model (10.8 ± 1.4 vs 5.9 ± 0.8 nmol DNPH/mg protein, P < 0.001), but no significant effect of the model was observed when the pork was seasoned with herbs. Lipid oxidation was not or was marginally affected by the installed model.