Oxidative cellular damage associated with transformation of Helicobacter pylori from a bacillary to a coccoid form

Exposure to unfavorable conditions results in the transformation of Helicob acter pylori, a gastric pathogen, from a bacillary form to a coccoid form. The mechanism and pathophysiological significance of this transformation re main unclear. The generation of the superoxide radical by H. pylori has pre viously been shown to inhibit the bactericidal action of nitric oxide, the concentration of which is relatively high in gastric juice. With the use of chemiluminescence probes, both the qualify and quantity of reactive oxygen species generated by H, pylori have now been shown to change markedly duri ng the transformation from the bacillary form to the coccoid form. The tran sformation of H. pylori was associated with oxidative modification of cellu lar proteins, including urease, an enzyme required for the survival of this bacterium in acidic gastric juice. Although the cellular abundance of urea se protein increased during the transformation, the specific activity of th e enzyme decreased and it underwent aggregation. Specific activities of bot h superoxide dismutase and catalase in H. pylori also decreased markedly du ring the transformation. The transformation of H. pylori was also associate d with oxidative modification of DNA, as revealed by the generation of 8-hy droxyguanine, and subsequent DNA fragment. These observations indicate that oxidative stress elicited by endogenously generated reactive oxygen specie s might play an important role in the transformation of H. pylori from the bacillary form to the coccoid form. (C) 2000 Elsevier Science Inc.