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Today exercise is viewed not only as a leisurely activity but also as an effective preventive and therapeutic tool in medicine.

Oxidants and Antioxidants in Medical Science

Further biomedical studies in exercise physiology and biochemistry reports that strenuous physical exercise might cause oxidative lipid damage in various tissues. View via Publisher. Save to Library. Create Alert. Share This Paper. Topics from this paper.

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Reactive Oxygen Species Exercise Organ. Glutathione peroxidase GPx activity Figure 3 increased significantly in sedentary control group compared to baseline. However, in the supplemented sedentary group and both the exercise groups its activity decreased significantly compared to sedentary control group, but no change noted between the exercise groups. However, no change in GPx activity in both the exercising groups. Catalase CAT activity Figure 4 increased significantly in sedentary control group compared to baseline. The sedentary and exercise groups supplemented with vitamin E showed significant decrease in catalase activity as compared to sedentary control group.

Cat activity was significantly decreased in the supplemented groups, both exercising and non exercising groups. DNA damage Figure 5 was significantly higher in exercising rats as compared to sedentary control; however, the DNA damage in supplemented exercise group is significantly lower as compared to the non-supplemented exercise group.

There was a significant increase in the DNA damage in exercising groups both supplemented and non supplemented, as compared to the sededentary groups, but the supplemented exercising group showed significant reduction in DNA damage as compared to the non supplemented exercise group. Dietary antioxidants play a crucial role in preventing the toxic effects of endogenous reactive oxygen species and studies support a protective role of vitamin E against oxidative stress induced by exercise [ 22 ]. In rats, deficiency in vitamin E can increase the susceptibility of these animals to oxidative stress induced toxicity and human studies have shown that vitamin E supplementation reduces the oxidative stress and lipid peroxidation induced by exercise [ 23 ].

Most studies suggest that stressors like exercise increases the free radical generation in the body which in turn stimulates the increased production of antioxidant enzymes GPx and SOD [ 24 ]. A balance between antioxidants and oxidant production ensures a protective cellular environment. SOD functions as one of the primary enzymatic antioxidant defense against highly reactive superoxide radicals. It catalyses the dismutation of superoxide into oxygen and H 2 O 2. Previous studies reported that increased levels of SOD activity in blood and muscle at rest are common in trained individuals, and SOD activity is increased in response to exercise interventions in a trained population [ 11 ].

Endurance training has been shown to increase SOD activity in skeletal muscle [ 26 , 27 ]. However, not all studies are consistent with these conclusions. This is consistent with our results which showed that the level of SOD is decreased in exercise group as compared to sedentary group.

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The reduction in SOD activity is unclear, but it could be due to the age related changes and also probably due to the activity of rats have been reduced during the 8 wks of the confinement in the cage. In reduce physical activity of rats the oxygen radical produced will be less and thus reducing the SOD activity. GPx belongs to peroxidase class of enzymes found in the erythrocytes of mammals that prevents lipid peroxidation of the cellular membrane. GPx reduces lipid hydroperoxides generated during the lipid peroxidation to their corresponding alcohols and reduces free hydrogen peroxide to water [ 29 ].

It has been reported that there is a significant correlation of GPx activity and weekly training in runners [ 30 ]. Ortenblad et al. In correspondence to our study, we found a significant decrease in the level of GPx activity in exercise group compared to sedentary group, with or without supplementation. GPx activity was also reported to decrease as a result of adaptive changes in trained rats compared to untrained rats [ 32 ]. Vitamin E has glutathione GSH sparing effect. GPx uses GSH and when there is sparing of GSH, action of GPx is not affected by exercise, so we would expect no change in the exercising group with and without vitamin e supplementation.

Reactive oxygen species itself can act as a signal during exercise which upregulates the expression of GPx to prevent the oxidative stress. Catalase is widely distributed in the cell, with the majority of the activity occurring in the mitochondria and peroxisomes.

Catalase activity in response to a single bout of exercise is variable.


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Catalase activity undergoes adaptive changes during the exercise [ 33 , 34 ]. Reports have also depicted that there is no difference in catalase activity levels following marathon running [ 12 ]. Our results also showed that the level of catalase activity decreased between the exercise group compared to sedentary group.

Comet assay showed that exercise groups had significantly increased DNA damage as compared to the sedentary group. Oxidative tissue damage in vitamin E deficient animals is exacerbated by endurance training and, conversely, it is reduced by high-dose vitamin E supplementation; also, preliminary studies in humans have demonstrated antioxidant protection by high-dose vitamin E supplementation [ 35 ]. This is consistent with the study done by Tsai et al, , on human study who reported an increase in DNA damage 24 hour post exercise that persisted through day 7 in response to a 42 km run average run time 3 hours [ 36 ].

This is in accordance with the human studies done earlier which found that supplementation with vitamin E for 8 weeks was effective in reducing DNA damage after an incremental exercise test to exhaustion in healthy non smokers aged between years [ 37 ].

Supplementation with vitamin E before the exercise seemed to have the good effect, leading the investigators to conclude that vitamin E prevents exercise-induced DNA damage [ 13 ]. Vitamin E prevents the leakage of the cellular enzymes and content due to ROS [ 35 ]. Free Rad Biol Med. Press, New York. Jackson M: Exercise and oxygen radical production by muscle. Handbook of oxidants and antioxidants in exercise.

Edited by: C. Sen, L. Packer and O. Edited by: Hanninen, O. Sies H: Oxidative stress: introductory remarks. Oxidative stress. Edited by: Sies, H. Diplock AT: Antioxidant nutrients and disease prevention: an overview. Am J Clin Nutr. Cohen G, Heikkila R: The generation of hydrogen peroxide, superoxide and hydroxyl radical by 6-hydroxydopamine dialuric acid and related cytotoxic agents. J Biol Chem. Sports, Health and Nutrition. Edited by: Katch, F. J Appl Physiol.

Oxidants and antioxidants in exercise.

Free Radic Biol Med. Int J Sport Nutr. Mol Cell Biochem. Bejma J, Ji L: Aging and acute exercise enhance free radical generation in rat skeletal muscle. Biochem Soc Trans. Mal J Biochem Mol Bio. Beyer WF, Fridovich I: Assaying for superoxide dismutase activity: some large consequences of minor changes in condition. Analyt Biochem. Paglia DE, Valentine WN: Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase.

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J Lab Clin med. Aebi H: Catalase in vitro. Methods in Enzymology. Int J Radiant Biol.