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Helicobacter pylori‐induced lipid peroxidation in peripheral blood lymphocytes
Author(s) -
Fan XUE G.,
Yakoob JAVED,
Chua ANDREW,
Fan XUE J.,
Keeling PAUL W. N.
Publication year - 1995
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1995.tb01113.x
Subject(s) - lipid peroxidation , pathogenesis , helicobacter pylori , catalase , superoxide dismutase , peripheral blood mononuclear cell , gastritis , lipid peroxide , thiobarbituric acid , chemistry , spirillaceae , immunology , in vitro , medicine , biology , biochemistry , oxidative stress
Several lines of evidence implicate Helicobacter pylori infection in the pathogenesis of gastritis and peptic ulceration. To investigate whether H. pylori can cause lipid peroxidation in lymphocytes in vitro and to look for experimental evidence of lipid peroxidation induced by H. pylori , the lipid peroxide (LPO) level in peripheral blood lymphocytes was measured using the thiobarbituric acid fluorescence method. In the absence of added H. pylori , the LPO level in lymphocytes was 0.133±0.033 nmol/10 6 cells, and in the co‐culture of H. pylori with peripheral blood mononuclear cells 0.340±0.097 nmol/ 10 6 cells. A significant difference was found between the two groups (p<0.001). Antioxidants, either superoxide dismutase or catalase, could inhibit LPO production in lymphocytes. The present data provide further evidence that H. pylori can induce lipid peroxidation, which may be responsible for the pathogenesis of H. pylori‐associated mucosal damage.