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Decreasing xanthine oxidase‐mediated oxidative stress prevents useful cellular adaptations to exercise in rats
Author(s) -
GomezCabrera MariCarmen,
Borrás Consuelo,
Pallardó Federico V.,
Sastre Juan,
Ji Li Li,
Viña Jose
Publication year - 2005
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2004.080564
Subject(s) - xanthine oxidase , allopurinol , oxidative stress , p38 mitogen activated protein kinases , mapk/erk pathway , chemistry , microbiology and biotechnology , reactive oxygen species , kinase , signal transduction , superoxide dismutase , endocrinology , medicine , enzyme , biochemistry , biology
Reactive oxygen or nitrogen species (RONS) are produced during exercise due, at least in part, to the activation of xanthine oxidase. When exercise is exhaustive they cause tissue damage; however, they may also act as signals inducing specific cellular adaptations to exercise. We have tested this hypothesis by studying the effects of allopurinol‐induced inhibition of RONS production on cell signalling pathways in rats submitted to exhaustive exercise. Exercise caused an activation of mitogen‐activated protein kinases (MAPKs: p38, ERK 1 and ERK 2), which in turn activated nuclear factor κB (NF‐κB) in rat gastrocnemius muscle. This up‐regulated the expression of important enzymes associated with cell defence (superoxide dismutase) and adaptation to exercise (eNOS and iNOS). All these changes were abolished when RONS production was prevented by allopurinol. Thus we report, for the first time, evidence that decreasing RONS formation prevents activation of important signalling pathways, predominantly the MAPK–NF‐κB pathway; consequently the practice of taking antioxidants before exercise may have to be re‐evaluated.