Document Detail

Adaptation to oxidative challenge induced by chronic physical exercise prevents Na+,K+-ATPase activity inhibition after traumatic brain injury.
MedLine Citation:
PMID:  19422810     Owner:  NLM     Status:  MEDLINE    
Physical exercise is likely to alter brain function and to afford neuroprotection in several neurological diseases. Although the favorable effects of physical exercise on traumatic brain injury (TBI) patients is well known, little information is available regarding the role of free radicals in the improvement induced by physical exercise in an experimental model of TBI induced by fluid percussion injury (FPI). Thus, we investigated whether 6 weeks of swimming training protects against oxidative damage (measured by protein carbonylation and thiobarbituric acid-reactive substances-TBARS) and neurochemical alterations represented by immunodetection of alpha subunit and activity of Na(+),K(+)-ATPase after FPI in cerebral cortex of rats. Statistical analysis revealed that physical training protected against FPI-induced TBARS and protein carbonylation increase. In addition, physical training was effective against Na(+),K(+)-ATPase enzyme activity inhibition and alpha(1) subunit level decrease after FPI. Pearson's correlation analysis revealed that the decrease in levels of catalytic alpha(1) subunit of Na(+),K(+)-ATPase induced FPI correlated with TBARS and protein carbonylation content increase. Furthermore, the effective protection exerted by physical training against FPI-induced free radical correlated with the immunocontent of the catalytic alpha(1) subunit maintenance. These data suggest that TBI-induced reactive oxygen species (ROS) generation decreases Na(+),K(+)-ATPase activity by decreasing the total number of enzyme molecules, and that physical exercise protects against this effect. Therefore, the effective protection of selected targets, such as Na(+),K(+)-ATPase induced by physical training, supports the idea that physical training may exert prophylactic effects on neuronal cell dysfunction and damage associated with TBI.
Frederico Diniz Lima; Mauro Schneider Oliveira; Ana Flávia Furian; Mauren Assis Souza; Leonardo Magno Rambo; Leandro Rodrigo Ribeiro; Luiz Fernando Almeida Silva; Leandro Thies Retamoso; Maurício Scopel Hoffmann; Danieli Valnes Magni; Leticia Pereira; Michele Rechia Fighera; Carlos Fernando Mello; Luiz Fernando Freire Royes
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-05-05
Journal Detail:
Title:  Brain research     Volume:  1279     ISSN:  1872-6240     ISO Abbreviation:  Brain Res.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-22     Completed Date:  2009-09-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  147-55     Citation Subset:  IM    
Centro de Ciências da Saúde, Departamento de Fisiologia, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
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MeSH Terms
Analysis of Variance
Body Weight
Brain Injuries / enzymology*,  physiopathology
Cerebral Cortex / enzymology*,  physiopathology
Lactic Acid / blood
Oxidative Stress / physiology*
Physical Conditioning, Animal / physiology*
Protein Carbonylation
Random Allocation
Rats, Wistar
Sodium-Potassium-Exchanging ATPase / metabolism*
Thiobarbituric Acid Reactive Substances / metabolism
Reg. No./Substance:
0/Thiobarbituric Acid Reactive Substances; 50-21-5/Lactic Acid; EC ATPase

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