Adaptation to oxidative challenge induced by chronic physical exercise prevents Na+,K+-ATPase activity inhibition after traumatic brain injury.
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.
Centro de Ciências da Saúde, Departamento de Fisiologia, Universidade Federal de Santa Maria, Santa Maria, RS, Brazil.
Frederico Diniz
FD
Lima
Mauro Schneider
MS
Oliveira
Ana Flávia
AF
Furian
Mauren Assis
MA
Souza
Leonardo Magno
LM
Rambo
Leandro Rodrigo
LR
Ribeiro
Luiz Fernando Almeida
LF
Silva
Leandro Thies
LT
Retamoso
Maurício Scopel
MS
Hoffmann
Danieli Valnes
DV
Magni
Leticia
L
Pereira
Michele Rechia
MR
Fighera
Carlos Fernando
CF
Mello
Luiz Fernando Freire
LF
Royes
D000704:Analysis of Variance; D000818:Animals; D001835:Body Weight; D001930:Brain Injuries / Q000201:enzymology* / Q000503:physiopathology; D002540:Cerebral Cortex / Q000201:enzymology* / Q000503:physiopathology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D018384:Oxidative Stress / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D050050:Protein Carbonylation; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D013550:Swimming; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
D017392:Thiobarbituric Acid Reactive Substances; D019344:Lactic Acid; D000254:Sodium-Potassium-Exchanging ATPase