Swim training attenuates oxidative damage and promotes neuroprotection in cerebral cortical slices submitted to oxygen glucose deprivation

• Published in: Journal of neurochemistry Vol. 123; no. 2; pp. 317 - 324
• Main Authors: Leite, Hércules R., Mourão, Flávio A. G., Drumond, Luciana E., Ferreira-Vieira, Talita H., Bernardes, Danielle, Silva, Josiane F., Lemos, Virgínia S., Moraes, Márcio F. D., Pereira, Grace S., Carvalho-Tavares, Juliana, Massensini, André R.
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell Publishing Ltd 01.10.2012; Wiley-Blackwell
• Subjects: Animals; Antioxidants; Biological and medical sciences; Brain; Brain slice preparation; Cell Hypoxia - physiology; Cerebral Cortex - metabolism; Cerebral Cortex - pathology; Data processing; exercise; Glucose; Glucose - deficiency; Glucose - metabolism; Glutamic acid; Ischemia; L-Lactate dehydrogenase; Lipid membranes; Male; Medical sciences; Neurology; Neuropharmacology; Neuroprotection; Neuroprotective agent; Nitric oxide; Nitrite; Organ Culture Techniques; Oxidative stress; Oxidative Stress - physiology; Oxygen; Oxygen - metabolism; Pharmacology. Drug treatments; Physical Conditioning, Animal - methods; Physical Conditioning, Animal - physiology; Physical training; Rats; Rats, Wistar; Superoxide dismutase; Swimming - physiology; Vascular diseases and vascular malformations of the nervous system; Oxidative stress; Cerebral cortex; Oxygen; Deprivation; Rat; Rodentia; Central nervous system; Cardiovascular disease; Male; exercise; Glucose; Antioxidant; Glutamate; Encephalon; ischemia; Vertebrata; Mammalia; Animal; Nitric oxide; neuroprotection; Excitatory aminoacid; Neurotransmitter; Release
• ISSN: 0022-3042; 1471-4159
• DOI: 10.1111/j.1471-4159.2012.07898.x

Although it is well known that regular exercise may promote neuroprotection, the mechanisms underlying this effect are still not fully understood. We investigated if swim training promotes neuroprotection by potentiating antioxidant pathways, thereby decreasing the effects of oxidative stress on glutamate and nitric oxide release. Male Wistar rats (n=36) were evenly randomized into a trained group (TRA) (5 days/week, 8 weeks, 30 min) and a sedentary group (SED). Forty‐eight hours after the last session of exercise, animals were killed and brain was collected for in vitro ischemia. Cortical slices were divided into two groups: a group in which oxidative stress was induced by oxygen and glucose deprivation (OGD), and a group of non‐deprived controls (nOGD). Interestingly, exercise by itself increased superoxide dismutase activity (nOGD, SED vs. TRA animals) with no effect on pro‐oxidative markers. In fact, TRA‐OGD slices showed lowered levels of lactate dehydrogenase when compared with SED‐OGD controls, reinforcing the idea that exercise affords a neuroprotective effect. We also demonstrated that exercise decreased glutamate and nitrite release as well as lipid membrane damage in the OGD cortical slices. Our data suggest that under conditions of metabolic stress, swim training prevents oxidative damage caused by glutamate and nitric oxide release. Swim training and cortical neuroprotection.The mechanisms underlying neuroprotective effects of regular exercise are still not fully understood. Here, we showed that swim training promotes neuroprotection decreasing the effects of oxidative stress on lipid membrane damage, as well as, on glutamate and nitric oxide release from brain cortical slices. Our data reinforce the idea that exercise affords a neuroprotective effect.