Evasion of the toxic effects of oxygen

Textbook (chapter)


Hazell, Stuart L., Harris, Andrew G. and Trend, Mark A.. 2001. "Evasion of the toxic effects of oxygen." Mobley, Harry L. T., Mendz, George L. and Hazell, Stuart L. (ed.) Helicobacter pylori: physiology and genetics. United States. American Society for Microbiology. pp. 167-178
Chapter Title

Evasion of the toxic effects of oxygen

Book Chapter CategoryTextbook (chapter)
ERA Publisher ID1124
Book TitleHelicobacter pylori: physiology and genetics
AuthorsHazell, Stuart L. (Author), Harris, Andrew G. (Author) and Trend, Mark A. (Author)
EditorsMobley, Harry L. T., Mendz, George L. and Hazell, Stuart L.
Page Range167-178
Number of Pages12
Year2001
PublisherAmerican Society for Microbiology
Place of PublicationUnited States
ISBN1555812139
Web Address (URL)http://www.ncbi.nlm.nih.gov/books/NBK2416/?report=printable
Abstract

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.

ANZSRC Field of Research 2020320103. Respiratory diseases
310106. Enzymes
310799. Microbiology not elsewhere classified
Public Notes

Chaptrer 15

Byline AffiliationsUniversity of Western Sydney
Institution of OriginUniversity of Southern Queensland
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