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Adaptive Redox Response to Oxidative Challenge during Exercise: Potential Roles of Nrf2 and HO‐1
Author(s) -
Kim SiYoung,
Lee YoungSoo,
Surh YoungJoon
Publication year - 2011
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.25.1_supplement.1107.11
Subject(s) - oxidative stress , glutathione , heme oxygenase , reactive oxygen species , antioxidant , chemistry , oxidative phosphorylation , heme , transcription factor , p50 , medicine , endocrinology , biochemistry , biology , enzyme , gene
There has been considerable accumulation of evidence supporting that exhaustive exercise causes oxidative stress through the formation of reactive oxygen species. However, our body tends to adapt to oxidative stress via antioxidant defense. One of the central components of the cellular antioxidant defense system is heme oxygenase‐1 (HO‐1). Induction of HO‐1 is known to be mediated by stress response elements or antioxidant response elements which are under the control of the redox sensitive transcription factor NF‐E2‐related factor‐2 (Nrf2). To determine whether induction of the oxidative stress can provoke adaptive antioxidative responses during exercise, the levels of glutathione (GSH), expression of HO‐1 and activation of Nrf2 were examined. The DNA binding activity of Nrf2 and expression of HO‐1 in human peripheral blood mononuclear cells (PBMCs) and/or mouse tissues were substantially increased after exercise in comparison with those achieved under resting conditions, while the levels of GSH in erythrocyte declined. However, Nrf2‐DNA binding activity and HO‐1 expression as well as GSH levels returned completely to the basal levels during the resting period. In another experiment, after exercise training for 12 weeks, the HO‐1 expression and Nrf2 activation in volunteers subjected to high‐intensity exercise were more pronounced than those observed by sedentary and low‐intensity exercise. Taking all these findings into account, we conclude that Nrf2 activation and subsequent expression of HO‐1 are induced differentially depending on the intensity and duration of exercise.