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Mice expressing Cre recombinase under control of the parietal cell Atpase4b gene promoter were crossed with mice harboring loxP sequences flanking the sod2 gene (SOD2 floxed mice). Cre-positive mice and Cre-negative littermates (controls) were used in studies of SOD2 expression, parietal cell function (ATP synthesis, acid secretion, and mitochondrial enzymatic activity), increased oxidative\/nitrosative stress, and gastric susceptibility to acute injury. Parietal cell SOD2 deficiency was accompanied by a 20% ( P &lt; 0.05) reduction in total gastric SOD activity and a 93% ( P &lt; 0.001) reduction in gastric SOD2 activity. In SOD2-deficient mice, mitochondrial aconitase and ATP synthase activities were impaired by 36% ( P &lt; 0.0001) and 44% ( P &lt; 0.005), respectively. Gastric tissue ATP content was reduced by 34% ( P &lt; 0.002). Basal acid secretion and peak secretagogue (histamine)-induced acid secretion were reduced by 43% ( P &lt; 0.0001) and 40% ( P &lt; 0.0005), respectively. There was a fourfold ( P &lt; 0.02) increase in gastric mucosal apoptosis and 41% ( P &lt; 0.001) greater alcohol-induced gastric damage in the parietal cell SOD2-deficient mice. Our findings indicate that loss of parietal cell SOD2 leads to mitochondrial dysfunction, resulting in perturbed energy metabolism, impaired parietal cell function, and increased gastric mucosal oxidative stress. 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