Evasion of the toxic effects of oxygen

Hazell, Stuart L. and Harris, Andrew G. and Trend, Mark A. (2001) Evasion of the toxic effects of oxygen. In: Helicobacter pylori: physiology and genetics. American Society for Microbiology, United States, pp. 167-178. ISBN 1-55581-213-9

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Oxygen is an efficient terminal electron acceptor in respiratory pathways. During aerobic respiration the electron transport chain generates free radical oxygen species as a result of electron leakage; this generation of toxic species is proportional to the oxygen tension (51). In addition, toxic oxygen species (TOS) may be formed exogenously, for example, by chemical processes or through radiation. TOS also result from the oxidative burst of polymorphonuclear leukocytes (PMN). Infection with Helicobacter pylori induces an inflammatory response (gastritis), which leads to an increase in the level of TOS in the gastric mucosa and the gastric juice (4, 24–26, 59). This increase in the level of toxic metabolites is probably the result of the generation of the superoxide anion (O2·− ), a reactive TOS, formed as part of the oxidative burst of PMN and enzymic activities of gastric epithelial cells. There is evidence that H. pylori infection leads to increased production of O2·− via NADPH oxidase in gastric cells, stimulated by lipopolysaccharide as well as xanthine oxidase, another mechanism for the generation of oxygen-derived free radicals (8, 80). In response to increased superoxide anion production in gastric tissue, changes have been detected in the level of expression of human superoxide dismutase (SOD) (12). Human gastric SOD exists as a cytoplasmic copper-zinc-superoxide dismutase (Cu, Zn-SOD) found in gland cells of the gastric body and antral mucosa, and as a manganese-superoxide dismutase (Mn-SOD) within mitochondria (63). An increase in the amount and activity of Mn-SOD has been observed in response to H. pylori infection and gastritis, whereas the amount and activity of the Cu, Zn-SOD remained constant or decreased slightly (39). It has been suggested that the induction of Mn-SOD is in response to increased cytokine production within the inflamed gastric mucosa (39). This situation is reversed following successful treatment of the infection (38). The data suggest that within the gastric environment H. pylori may be exposed to increased levels of TOS. In such an environment it is important for bacterial survival that the impact of such TOS be neutralized.

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Item Type: Book Chapter (Commonwealth Reporting Category B)
Refereed: Yes
Item Status: Live Archive
Additional Information: Chaptrer 15
Faculty/School / Institute/Centre: Historic - Faculty of Sciences - Department of Biological and Physical Sciences (Up to 30 Jun 2013)
Faculty/School / Institute/Centre: Historic - Faculty of Sciences - Department of Biological and Physical Sciences (Up to 30 Jun 2013)
Date Deposited: 13 Mar 2018 02:07
Last Modified: 05 Apr 2018 05:54
Fields of Research (2008): 11 Medical and Health Sciences > 1102 Cardiovascular Medicine and Haematology > 110203 Respiratory Diseases
06 Biological Sciences > 0601 Biochemistry and Cell Biology > 060107 Enzymes
06 Biological Sciences > 0605 Microbiology > 060599 Microbiology not elsewhere classified
Fields of Research (2020): 32 BIOMEDICAL AND CLINICAL SCIENCES > 3201 Cardiovascular medicine and haematology > 320103 Respiratory diseases
31 BIOLOGICAL SCIENCES > 3101 Biochemistry and cell biology > 310106 Enzymes
31 BIOLOGICAL SCIENCES > 3107 Microbiology > 310799 Microbiology not elsewhere classified
Socio-Economic Objectives (2008): E Expanding Knowledge > 97 Expanding Knowledge > 970106 Expanding Knowledge in the Biological Sciences
URI: http://eprints.usq.edu.au/id/eprint/21507

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