PMID- 15256219
OWN - NLM
STAT- MEDLINE
DCOM- 20050131
LR  - 20220317
IS  - 0891-5849 (Print)
IS  - 0891-5849 (Linking)
VI  - 37
IP  - 4
DP  - 2004 Aug 15
TI  - Oxidative stress and delayed-onset muscle damage after exercise.
PG  - 480-7
AB  - Reactive oxygen species (ROS) produced during exercise may be involved in 
      delayed-onset muscle damage related to inflammation. To investigate this 
      hypothesis, we studied whether oxidative stress increases nuclear translocation 
      of nuclear factor-kappaB and chemokine expression in skeletal muscle using 
      myotube L6 cells. We also assessed whether prolonged acute exercise could 
      increase these parameters in rats. In L6 cells, H(2)O(2) induced nuclear 
      translocation of p65 and increased the expression of cytokine-induced neutrophil 
      chemoattractant-1 (CINC-1) and monocyte chemoattractant protein-1 (MCP-1), 
      whereas preincubation with alpha-tocopherol limited the increase in these 
      proteins. Sprague Dawley rats were divided into the following groups: rested 
      control, exercised, rested with a high alpha-tocopherol diet, and exercised with 
      a high alpha-tocopherol diet. After 3 weeks of acclimation, both exercise groups 
      ran on a treadmill at 25 m/min for 60 min. Exercise increased nuclear p65, 
      CINC-1, and MCP-1 in gastrocnemius muscle cells, but these changes were 
      ameliorated by the high alpha-tocopherol diet. Increases in myeloperoxidase and 
      thiobarbituric acid-reactive substrates were ameliorated by a high 
      alpha-tocopherol diet, as were the histological changes. Neutrophil activity was 
      not altered by either exercise or a high alpha-tocopherol diet. These results 
      indicate that delayed-onset muscle damage induced by prolonged exercise is partly 
      related to inflammation via phagocyte infiltration caused by ROS and that 
      alpha-tocopherol (an antioxidant) can attenuate such inflammatory changes.
FAU - Aoi, Wataru
AU  - Aoi W
AD  - Department of Inflammation and Immunology, Graduate School of Medical Science, 
      Kyoto Prefectural University of Medicine, Kyoto, 602-8566, Japan. 
      waoi@koto.kpu-m.ac.jp
FAU - Naito, Yuji
AU  - Naito Y
FAU - Takanami, Yoshikazu
AU  - Takanami Y
FAU - Kawai, Yukari
AU  - Kawai Y
FAU - Sakuma, Kunihiro
AU  - Sakuma K
FAU - Ichikawa, Hiroshi
AU  - Ichikawa H
FAU - Yoshida, Norimasa
AU  - Yoshida N
FAU - Yoshikawa, Toshikazu
AU  - Yoshikawa T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Free Radic Biol Med
JT  - Free radical biology & medicine
JID - 8709159
RN  - 0 (Antioxidants)
RN  - 0 (Calcium-Binding Proteins)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Synaptotagmin I)
RN  - 0 (Thiobarbituric Acid Reactive Substances)
RN  - 134193-27-4 (Synaptotagmins)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 1.11.1.7 (Peroxidase)
RN  - H4N855PNZ1 (alpha-Tocopherol)
SB  - IM
MH  - Active Transport, Cell Nucleus
MH  - Animals
MH  - Antioxidants/pharmacology
MH  - Calcium-Binding Proteins/metabolism
MH  - Cell Line
MH  - Chemokine CCL2/metabolism
MH  - Chemokines/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Hydrogen Peroxide/pharmacology
MH  - Inflammation
MH  - Membrane Glycoproteins/metabolism
MH  - Mice
MH  - Muscle, Skeletal/injuries/metabolism/*pathology
MH  - NF-kappa B/metabolism
MH  - Nerve Tissue Proteins/metabolism
MH  - Neutrophils/metabolism
MH  - Oxidation-Reduction
MH  - *Oxidative Stress
MH  - Peroxidase/metabolism
MH  - Physical Conditioning, Animal
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reactive Oxygen Species
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Synaptotagmin I
MH  - Synaptotagmins
MH  - Thiobarbituric Acid Reactive Substances/metabolism
MH  - Time Factors
MH  - Transcription, Genetic
MH  - alpha-Tocopherol/pharmacology
EDAT- 2004/07/17 05:00
MHDA- 2005/02/03 09:00
CRDT- 2004/07/17 05:00
PHST- 2003/11/04 00:00 [received]
PHST- 2004/03/31 00:00 [revised]
PHST- 2004/05/07 00:00 [accepted]
PHST- 2004/07/17 05:00 [pubmed]
PHST- 2005/02/03 09:00 [medline]
PHST- 2004/07/17 05:00 [entrez]
AID - S0891584904003910 [pii]
AID - 10.1016/j.freeradbiomed.2004.05.008 [doi]
PST - ppublish
SO  - Free Radic Biol Med. 2004 Aug 15;37(4):480-7. doi: 
      10.1016/j.freeradbiomed.2004.05.008.