Single bout of exercise eliminates the immobilization-induced oxidative stress in rat brain (original) (raw)
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Oxidative Stress Induced by Intense and Exhaustive Exercise Impairs Murine Cognitive Function
Journal of Neurophysiology, 2007
It has been shown that exercise is helpful against brain disorders. However, this may not be true for intense exercise (IE). Because it is easy to misadjust exercise intensity with physical condition, it is essential to know the effects of IE on cognitive process because it may have important consequences on people skills and work skills. We investigated the effects of IE on male C57Bl/6 mice, 3-mo-old, undergoing 10 days of intense and exhaustive running program on cognition and its possible relationship with brain oxidative stress. Cognition was evaluated by three different cognitive tests: passive avoidance task, contextual fear conditioning, and tone fear conditioning, performed 24 h after the last exercise session. Brain oxidative stress was evaluated by lipid peroxidation and protein oxidation. There was a remarkable memory reduction of exercised animals in comparison with the control group, associated with increase in the brain oxidative stress, with no alterations in shock s...
Neurochemistry International, 2006
In the current investigation we tested how swimming training (T) (8 week, 5 times/week, 2 h/day), and detraining (DT) affects brain functions and oxidative stress markers in rat brain. The free radical concentration, measured by electron paramagnetic resonance, decreased in brain of T and DT rats compared to controls (C). The level of brain-derived neurotrophic factor (BDNF) increased as a result of training, but decreased below the control level after 6 weeks of detraining. In addition, the concentration of nerve growth factor (NGF) also declined with DT. The passive avoidance test was used to assess the memory of rats, and training-induced improvement was observed but the enhancement disappeared with detraining. When the content of mitochondrial electron transport complexes, as a potent free radical generator, was evaluated by the blue native gel method, no significant alterations were observed. The repair of nuclear and mitochondrial 8-oxodeoxyguanosine, as measured by the activity of OGG1, showed no significant difference. Therefore, the results suggest that regular exercise training improves memory, decreases the level of reactive oxygen species, and increase the production of BDNF and NGF. On the other hand, it appears that the beneficial effects of training are reversible in the brain, since detraining down-regulates the neurotrophin level, and memory. It is suggested that exercise training is more likely to beneficially effect the production of reactive oxygen species and the related oxidative damage. #
Neuroscience Letters, 2006
Although regular physical exercise is beneficial to the body, it is well known that exhaustive exercise causes oxidative stress in muscle. Recent studies suggest that regular moderate physical exercise has the beneficial effects on brain. However, there is little information regarding whether or not exhaustive exercise could generate oxidative stress in brain and the findings are conflicting. The aim of this study was to investigate the effects of exhaustive exercise on thiobarbituric acid reactive substances, as an indicator of lipid peroxidation, in the hippocampus, prefrontal cortex and striatum. Additionally we examined antioxidant enzymes activities, superoxide dismutase and glutathione peroxidase, to assess the effects of reactive oxygen species. Exhaustive exercise did not change superoxide dismutase and glutathione peroxidase enzyme activities and thiobarbituric acid reactive substances levels neither immediately (0 min) nor at 3, 6, 12, 24 and 48 h after the cessation of exercise in the brain. These results indicate that acute exhaustive exercise may not cause significant lipid peroxidation in the hippocampus, prefrontal cortex and striatum during the post-exercise period.
Neurochemistry International - NEUROCHEM INT, 2005
We have tested the hypothesis that training with moderate- (MT), strenuous- (ST), or over- (OT) load can cause alterations in memory, lipid peroxidation, protein oxidation, DNA damage, activity of 8-oxoG-DNA glycosylase (OGG1) and brain-derived neurotrophic factor (BDNF), in rat brain. Rat memory was assessed by a passive avoidance test and the ST and OT group demonstrated improved memory. The content of BDNF was increased only in the OT group. The oxidative damage of lipids and DNA, as measured by thiobarbituric acid reactive substances (TBARS), and 8-hydroxydeoxyguanosine (8-OHdG), did not change significantly with exercise. Similarly, the activity of DNA repair enzyme, 8-oxoguanine DNA glycosylase (OGG1), was not altered with exercise training. On the other hand, the content of reactive carbonyl derivatives (RCDs) decreased in all groups and the decrease reached significance levels in the ST and OT groups. The activity of the proteasome complex increased in the brain of OT. The f...
Brain Research, 2008
Daily moderate intensity exercise (2 weeks of 20 min/day of treadmill training), which reduces damage to hippocampal slices from rats submitted to in vitro ischemia, did not modify oxidative stress parameters in the hippocampus nor the brain-derived neurotrophic factor (BDNF) levels in different brain regions. The aim was to investigate whether the modulation of hippocampal oxidative status and/or brain BDNF content is involved in exercise-induced neuroprotection. Wistar rats were submitted to daily exercise in the treadmill and were sacrificed approximately 16 h after the last treadmill running. Some several oxidative stress parameters were determined, specifically the free radical levels, the macromolecule damage, the total reactive antioxidant potential and reactivity levels, which represent the total antioxidant capacity, in the hippocampus. In addition, BDNF levels in different rat cerebral regions (hippocampus, cortex, striatum, and the cerebellum) were measured by ELISA. The used exercise protocol did not affect any oxidative stress parameters studied in the hippocampus, suggesting that it does not cause a significant oxidative stress nor induce adaptations of the cellular antioxidant system. Treadmill training also did not change the BDNF content in brain areas studied. Considering the fact that this exercise protocol have been shown to be neuroprotective, we might speculate that BDNF levels and oxidative status may not be directly involved with the mechanisms of exercise-induced neuroprotection after ischemia.
Physical Exercise Improves Total Antioxidant Capacity and Gene Expression in Rat Hippocampal Tissue
Archives italiennes de biologie, 2017
Exercise may exert beneficial effects on cognitive functions and play an important role in the prevention of neurodegenerative diseases. Such effects seem to be mediated by changes in anti-oxidative status, but limited information is available on the nature of molecular pathways supporting the antioxidant effects of exercise in the brain. In this study 3-5-month-old male Wistar albino rats were subjected to three times/week moderate intensity exercise on a rodent treadmill for a period of 6 weeks. The tissue antioxidant activity towards various reactive oxygen species (ROS) was determined in the hippocampus. In addition, to identify the molecular pathways that may be involved in ROS metabolism, the expression of nerve growth factor (NGF) and sirtuins (SIRT1 and SIRT3) were measured. Our results showed a higher antioxidant activity in the hippocampus of physically trained rats compared to sedentary controls. Furthermore, exercise induced an up-regulation of NGF, possibly related to a...
The complex role of physical exercise and reactive oxygen species on brain
Journal of Sport and Health Science, 2013
Reactive oxygen species (ROS) are continuously generated during aerobic metabolism and at moderate level. They play a role in redox signaling, but in significant concentration they cause oxidative damage and neurodegeneration. Because of the enhanced sensitivity of brain to ROS, it is especially important to maintain the normal redox state in different types of neuron cells. In last decade it became clear that regular exercise beneficially affects brain function, and can play an important preventive and therapeutic role in stroke, Alzheimer, and Parkinson diseases. The effects of exercise appear to be very complex and could include neurogenesis via neurotrophic factors, increased capillariszation, decreased oxidative damage, and increased proteolytic degradation by proteasome and neprilysin. Data from our and other laboratories indicate that exercise-induced modulation of ROS levels plays a role in the protein content and expression of brain-derived neurotrophic factor, tyrosinerelated kinase B (TrkB), and cAMP response element binding protein, resulting in better function and increased neurogenesis. Therefore, it appears that exercise-induced modulation of the redox state is an important means, by which exercise benefits brain function, increases the resistance against oxidative stress, facilitates recovery from oxidative stress, and attenuates age-associated decline in cognition.
Neurobiological effects of forced swim exercise on the rodent hippocampus: a systematic review
Acta Neurobiologiae Experimentalis, 2021
Forced swimming is a common exercise method used for its low cost and easy management, as seen in studies with the hippocampus. Since it is applied for varied research purposes many protocols are available with diverse aspects of physical intensity, time and periodicity, which produces variable outcomes. In the present study, we performed a systematic review to stress the neurobiological effects of forced swim exercise on the rodent hippocampus. Behavior, antioxidant levels, neurotrophins and inflammatory markers were the main topics examined upon the swimming effects. Better results among these analyses were associated with forced exercise at moderate intensity with an adaptation period and the opposite for continuous exhausting exercises with no adaptation. On further consideration, a standard swimming protocol is necessary to reduce variability of results for each scenario investigated about the impact of the forced swimming on the hippocampus.