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      Oxidative stress and antioxidant defense mechanisms linked to exercise during cardiopulmonary and metabolic disorders

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          Abstract

          Oxidative stress has been implicated in the pathophysiology of multiple human diseases, in addition to the aging process. Although various stimuli exist, acute exercise is known to induce a transient increase in reactive oxygen and nitrogen species (RONS), evident by several reports of increased oxidative damage following acute bouts of aerobic and anaerobic exercise. Although the results are somewhat mixed and appear disease dependent, individuals with chronic disease experience an exacerbation in oxidative stress following acute exercise when compared to healthy individuals. However, this increased oxidant stress may serve as a necessary “signal” for the upregulation in antioxidant defenses, thereby providing protection against subsequent exposure to prooxidant environments within susceptible individuals. Here we present studies related to both acute exercise-induced oxidative stress in those with disease, in addition to studies focused on adaptations resulting from increased RONS exposure associated with chronic exercise training in persons with disease.

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          Most cited references70

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          Postprandial hyperglycemia and diabetes complications: is it time to treat?

          A Ceriello (2004)
          Increasing evidence suggests that the postprandial state is a contributing factor to the development of atherosclerosis. In diabetes, the postprandial phase is characterized by a rapid and large increase in blood glucose levels, and the possibility that the postprandial "hyperglycemic spikes" may be relevant to the onset of cardiovascular complications has recently received much attention. Epidemiological studies and preliminary intervention studies have shown that postprandial hyperglycemia is a direct and independent risk factor for cardiovascular disease (CVD). Most of the cardiovascular risk factors are modified in the postprandial phase in diabetic subjects and directly affected by an acute increase of glycemia. The mechanisms through which acute hyperglycemia exerts its effects may be identified in the production of free radicals. This alarmingly suggestive body of evidence for a harmful effect of postprandial hyperglycemia on diabetes complications has been sufficient to influence guidelines from key professional scientific societies. Correcting the postprandial hyperglycemia may form part of the strategy for the prevention and management of CVDs in diabetes.
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            Chronic inflammation and cancer.

            A substantial body of evidence supports the conclusion that chronic inflammation can predispose an individual to cancer, as demonstrated by the association between chronic inflammatory bowel diseases and the increased risk of colon carcinoma. Chronic inflammation is caused by a variety of factors, including bacterial, viral, and parasitic infections, chemical irritants, and nondigestible particles. The longer the inflammation persists, the higher the risk of associated carcinogenesis. This review describes some of the underlying causes of the association between chronic inflammation and cancer. Inflammatory mediators contribute to neoplasia by inducing proneoplastic mutations, adaptive responses, resistance to apoptosis, and environmental changes such as stimulation of angiogenesis. All these changes confer a survival advantage to a susceptible cell. In this article, we discuss the contribution of reactive oxygen and nitrogen intermediates, prostaglandins, and inflammatory cytokines to carcinogenesis. A thorough understanding of the molecular basis of inflammation-associated neoplasia and progression can lead to novel approaches to the prevention and treatment of cancer.
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              Oxidants in cigarette smoke. Radicals, hydrogen peroxide, peroxynitrate, and peroxynitrite.

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                Author and article information

                Journal
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Landes Bioscience
                1942-0900
                1942-0994
                Jan-Mar 2009
                : 2
                : 1
                : 43-51
                Affiliations
                Cardiorespiratory/Metabolic Laboratory; The University of Memphis; Memphis, Tennessee USA
                Author notes
                Correspondence to: Richard J. Bloomer; Cardiorespiratory/Metabolic Laboratory; 161F Elma Neal Roane Field House; The University of Memphis; Memphis, Tennessee 38152 USA; Tel.: 901.678.4341; Fax: 901.678.3591; Email: rbloomer@ 123456memphis.edu
                Article
                1942-0900-2-1-8
                10.4161/oxim.2.1.7732
                2763230
                20046644
                78015d12-57bb-44e4-b676-9af795221690
                Copyright © 2009 Landes Bioscience
                History
                : 11 December 2008
                : 17 December 2008
                : 18 December 2008
                Categories
                Review

                Molecular medicine
                obesity,cigarette smoking,exercise,chronic obstructive pulmonary disease,diabetes,antioxidant,reactive oxygen species,cardiovascular disease

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