Adaptation to oxidative challenge induced by chronic physical exercise prevents Na+,K+-ATPase activity inhibition after traumatic brain injury

Exercise Pre-conditioning Reduces Brain Inflammation and Protects against Toxicity Induced by Traumatic Brain Injury: Behavioral and Neurochemical Approach

“…,K ? -ATPase activity (Lima et al 2009) and showed the involvement of the neutrophil infiltration (here characterized by MPO activity increase) and generation of inflammatory processes in the collapses of ion gradient homeostasis for the first time. In addition, Pearson's correlation analysis revealed strong correlation of MPO activity increase with Na ?…”

The effects of treadmill exercise on oxidative stress in Mongolian gerbils with penicillin-induced epilepsy

“…In the course of this knowledge and experience, it has been shown that regularly exercising animals and people are receiving responses to improving endurance capacity by reducing oxidant production and increasing antioxidant defense mechanisms and mitochondrial biogenesis [34,35]. Therefore, they are the neuroprotective effects of aerobic exercise training [36,37]. In addition, exercise also increases the expression and levels of neurotrophic and growth factors such as Insulin-like growth factor 1, fibroblast growth factor 2 and brain-derived neurotrophic factor [38][39][40].…”

The involvement of Na+, K+-ATPase activity and free radical generation in the susceptibility to pentylenetetrazol-induced seizures after experimental traumatic brain injury

“…In addition, the total activity of superoxide dismutase (SOD) and the content of the antioxidant α-tocopherol have been found to be reduced in rat brain homogenates after acute PTZ-induced convulsion [49]. Previous studies from our group have demonstrated that the injection of PTZ-induced convulsive activity is accompanied by ROS generation and inhibition of local Na + ,K + -ATPase activity [50,51,13,22,52]reinforcing the assumption that the inhibition of some selected targets for free radicals increases cellular excitability [53][54][55].…”

“…After 30 min of incubation, samples were centrifuged (3000 ×g, 15 min) and then TBARS levels were measured at 532 nm according to Ohkawa et al [29]. For the protein carbonyl assay, the cortical tissues surrounding the injured core were homogenized in cold 10 mM Tris-HCl buffer (pH 7.4) and carbonyl protein content was determined by Yan et al [30] adapted for brain tissue by Lima et al [13]. Briefly, homogenates were diluted to 750-800 μg/ml of protein in each sample, and 1 ml aliquots were mixed with 0.2 ml of 2,4 dinitrophenylhydrazine (10 mM DNPH)or 0.2 ml HCl (2 M).…”

“…Recent studies have demonstrated that the oxidative damage mediated by reactive oxygen species (ROS) and nitrogen species (RNS) is a significant component of the secondary injury cascade that accompanies TBI [7][8][9][10][11]. Although several evidences supporting the idea that any cellular constituent may be a target for free radical damage [12], the inhibition of some selected targets such as Na + ,-K + -ATPase may play an important role in the hyperexcitability induced by TBI [13]. Na + ,K + -ATPase is a membrane bound enzyme known to play a pivotal role in cellular ionic gradient maintenance and is particularly sensitive to reactive species [14,15].…”