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Effects of endurance physical training on hydroxyl radical generation in rat tissues

Physical exercise is known to increase oxygen consumption to compensate for enhanced ATP consumption and thus to induce oxidative stress in tissues. Our previous data indicate that training significantly increased the hydroxyl radical level in rat tissues after physical exercise, but reduced the bas...

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Published in:Life sciences (1973) 1998, Vol.63 (21), p.1921-1929
Main Authors: Itoh, Hiroshi, Ohkuwa, Tetsuo, Yamamoto, Takako, Sato, Yuzo, Miyamura, Miharu, Naoi, Makoto
Format: Article
Language:English
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Summary:Physical exercise is known to increase oxygen consumption to compensate for enhanced ATP consumption and thus to induce oxidative stress in tissues. Our previous data indicate that training significantly increased the hydroxyl radical level in rat tissues after physical exercise, but reduced the basal level in aged rats. This result suggests the paradoxical effect of physical training, which may be to increase or scavenge reactive oxygen species (ROS) generated by physical exercise. In this paper, the effects of training on the levels of hydroxyl radicals and the anti-oxidative glutathione system, were examined in rats. After 3 weeks' training, rats were sacrificed at rest or after treadmill running and the levels of hydroxyl radicals trapped with salicylic acid, reduced (GSH); and oxidized glutathione (GSSG) in tissues were quantified by high-performance liquid chromatography-electrochemical detection (HPLC-ECD). Endurance training reduced the basal level of hydroxyl radicals significantly in plasma and soleus muscle. In liver and brain a similar tendency was observed, but the difference was not statistically significant. In liver the basal level of GSH increased significantly after training. Slower training with longer duration reduced the basal levels of hydroxyl radical in plasma more markedly than more intense training. These results suggest that endurance exercise can increase the anti-oxidative capacity in rats.
ISSN:0024-3205
1879-0631
DOI:10.1016/S0024-3205(98)00468-8