Mechanism of strong resistance of Helicobacter pylori respiration to nitric oxide.
The aim of the present work is to elucidate the mechanism by which the respiration of Helicobacter pylori but not of Escherichia coli shows a strong resistance to nitric oxide (NO). Nitric oxide strongly but reversibly inhibited the oxygen consumption by sonicated membranes from H. pylori and Triton X-100-treated cells. Although the sensitivity of the H. pylori respiration to cyanide was low, it also increased after the treatment with Triton X-100. Kinetic analyses revealed that NO was rapidly degraded by E. coli and the Triton X-100-treated H. pylori, but not by the intact H. pylori. Thus, the low sensitivity to NO might reflect the low affinity of the cytochrome c oxidase for this radical within the membrane/lipid bilayers of H. pylori. Such properties of the oxidase in H. pylori membranes may, at least in part, underlie the mechanism by which this bacterium thrives in NO-enriched gastric juice.
Park
Ah-Mee
AM
Department of Biochemistry and Molecular Pathology, Osaka City University Medical School, 1-4-3 Asahimachi, Abeno, 545-8585, Osaka, Japan.
Nagata
Kumiko
K
Sato
Eisuke F
EF
Tamura
Toshihide
T
Shimono
Kunio
K
Inoue
Masayasu
M
D000255:Adenosine Triphosphate / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D024881:Drug Resistance, Bacterial; D004926:Escherichia coli / Q000187:drug effects / Q000378:metabolism; D016480:Helicobacter pylori / Q000187:drug effects* / Q000378:metabolism; D007700:Kinetics; D010101:Oxygen Consumption / Q000187:drug effects*; D013045:Species Specificity
D000255:Adenosine Triphosphate