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Severe Hypoxia Enhances Lymphocyte Apoptosis Induced by Oxidative Stress during Moderate Exercise
Author(s) -
Lin ChiaTe,
Wang Jongshyan
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1173.5
Subject(s) - oxidative stress , apoptosis , lymphocyte , caspase , hypoxia (environmental) , chemistry , endocrinology , medicine , immunology , programmed cell death , oxygen , biochemistry , organic chemistry
This study investigated how exercise combined with hypoxia affects lymphocyte apoptosis induced by oxidative stress and its underlying mechanisms. Eight sedentary men engaged six conditions in a normobaric hypoxia chamber for 1 hour: two normoxic exercise [i.e., strenuous exercise (SE, up to VO2max) and moderate exercise (ME, 50%VO2max) in 21% O2], two hypoxic exercise (i.e., ME in 12% and 15% O2), and two hypoxic conditions (i.e., 12% and 15% O2). Our results demonstrated that SE enhanced H2O2‐induced phosphatidylserine (PS) exposure of lymphocyte, which enhancement was accompanied by diminished mitochondrial transmembrane potential (MTP) as well as increased active caspase 3, 8, and 9 levels. Although ME combined with 12% O2 intervention also promoted PS exposure and caspase 3, 8, and 9 activation induced by H2O2, there was not significant change in H2O2‐induced lymphocyte PS exposure and caspases activation following ME combined with 15% O2 intervention. Therefore, we conclude that exposure of 12% O2, but not 15% O2, enhances lymphocyte apoptosis induced by H2O2 at performed ME, possible by promoting activation of caspases in lymphocyte.