The effects of antioxidants on exercise‐induced lipid peroxidation in patients with COPD

Ağaçdiken, Ayşen; Başyiğit, İlknur; Ozden, Meltem; Yıldız, Füsun; Ural, Dilek; Maral, Hale; Boyacı, Haşim; Ilgazlı, Ahmet; Komşuoğlu, Baki

doi:10.1111/j.1440-1843.2003.00526.x

Cited by 35 publications

(25 citation statements)

References 16 publications

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“…Increased oxidative stress has also been reported in COPD patients following both acute maximal7,8,10,41 and submaximal7,10 aerobic exercise. This has been the case with one exception,42 evident by reported increases in MDA,8,10 thiobarbituric acid-reactive substances (TBARS),7,41 protein oxidation (protein carbonyls),41 DNA damage (comet assay),10 phagocytic superoxide production,7,41 as well as changes in glutathione redox status7 and other components of the antioxidant defense system (e.g., total antioxidant status) 7.…”

Section: Acute Exercise-induced Oxidative Stress and Diseasementioning

confidence: 89%

Oxidative Stress and Antioxidant Defense Mechanisms Linked to Exercise During Cardiopulmonary and Metabolic Disorders

Fisher‐Wellman

Bell

Bloomer

2008

Oxidative Medicine and Cellular Longevity

114

101

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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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Section: Acute Exercise-induced Oxidative Stress and Diseasementioning

confidence: 89%

Oxidative Stress and Antioxidant Defense Mechanisms Linked to Exercise During Cardiopulmonary and Metabolic Disorders

Fisher‐Wellman

Bell

Bloomer

2008

Oxidative Medicine and Cellular Longevity

114

101

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“…However, several studies have suggested that acute exercise may increase oxidative stress (OS), such as the increase in plasma thiobarbituric acid-reactive substance (TBARS) in COPD patients (Heunks et al 1999;Couillard et al 2002;Agacdiken et al 2004). In addition, Pinho et al (2007) reported that chronic exercise training can induce OS at baseline in COPD patients, and Barreiro et al (2009) demonstrated that nitrosative stress in severe COPD had increased after chronic endurance exercise.…”

Section: Introductionmentioning

confidence: 99%

Urinary 8-Hydroxydeoxyguanosine Is a Potential Indicator for Estimating Pulmonary Rehabilitation-Induced Oxidative Stress in COPD Patients

Nemoto

Oh‐ishi

Itoh

et al. 2014

Tohoku J. Exp. Med.

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Chronic obstructive pulmonary disease (COPD) is the most common chronic lung disease and is an important cause of morbidity worldwide. The aim of this study was to evaluate whether pulmonary rehabilitation (PR) improves the oxidant/antioxidant imbalance, exercise capacity and health-related quality of life (HRQL) in patients with different stages of COPD. Eighteen stable COPD patients participated in 8-week PR; the exercise intensity was set at 70% of the V 4 O 2 peak. Subjects were divided into 2 groups: moderate to severe (stages II/III: n = 12) and very severe COPD with FEV 1 < 30% predicted (stage IV: n = 6). In patients at stages II/III, PR improved exercise capacity (6-minute walking test: 431.2 ± 26.6 vs. 489.1 ± 26.5 m, P < 0.01 and shuttle walking test: 329.2 ± 41.4 vs. 378.2 ± 41.5 m, P < 0.01) and HRQL, whereas no significant change was observed in erythrocyte lipid peroxidation and urinary 8-hydroxydeoxyguanosine, a marker for DNA damage. In contrast, PR for stage IV patients did not improve exercise capacity and HRQL, but significantly increased urinary 8-hydroxydeoxyguanosine (14.5 ± 1.7 vs. 24.3 ± 2.6 ng/mg Cr, P < 0.05). In both groups, erythrocyte antioxidants (superoxide dismutase, glutathione peroxidase, and catalase) did not change significantly after PR. Thus, urinary 8-hydroxydeoxyguanosine is a useful indicator for the PR-induced oxidative stress in COPD patients. In conclusion, appropriate exercise program in COPD patients can improve exercise capacity and HRQL without further increase of oxidative stress. However, PR for very severe COPD patients enhanced exercise-induced oxidative stress.

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“…The total antioxidative potential of the plasma reflects the ability of an individual to resist the oxidative stress. Ferric reducing ability of plasma (FRAP) evaluates plasma total antioxidant capacity due to known and unknown antioxidants in the plasma 10 Therefore in the present study significant reduction observed in total ferric reducing ability of plasma may be due to increased free radical activity either because of inflammation or complications that results in imbalance between antioxidant capacity and proxidant affecting lung function. Extensively amplified oxidant burden and declined individual antioxidant levels might be responsible for the observed significant fall in total antioxidant capacity of patients with lung disease.…”

Section: Aimsmentioning

confidence: 78%

Study of oxidative stress in relation with antioxidant status in chronic bronchitis

Raut¹

2012

Int Jour of Biomed Res

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Oxidative stress has been recognized as a central feature of smoke induced chronic bronchitis, where lipid peroxide plays an important role in inflammatory lung disease. Increased lipid peroxide increases epithelial permeability produced by cigarette smoke is likely to be mediated though depletion of the Total Antioxidant Capacity. Imbalance between oxidants and Total Anioxidant Capacity is also an established fact in these patients. 60 patients with chronic bronchitis included in the study. Their base line clinical examination, malondialdehyde (MDA), nitric oxide, alpha tochopherol and Total Antioxidant Capacity were measured. 100 healthy non-smokers' were served as controls. The mean malondialdehyde levels and nitric oxide in the patients at base line were higher than Controls (p<0.001). Plasma alpha-tocopherol and total antioxidant capacity were lower (p<0.001) in the patients compared to controls. The present study shows that initially the plasma lipid peroxide (MDA) levels were high and antioxidants. (alpha-tocopherol, total antioxidant capacity) were low in patients with chronic bronchitis. Our results suggest the presence of oxidative stress and decrease in total antioxidant capacity in chronic bronchitis.

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The effects of antioxidants on exercise‐induced lipid peroxidation in patients with COPD

Cited by 35 publications

References 16 publications

Oxidative Stress and Antioxidant Defense Mechanisms Linked to Exercise During Cardiopulmonary and Metabolic Disorders

Oxidative Stress and Antioxidant Defense Mechanisms Linked to Exercise During Cardiopulmonary and Metabolic Disorders

Urinary 8-Hydroxydeoxyguanosine Is a Potential Indicator for Estimating Pulmonary Rehabilitation-Induced Oxidative Stress in COPD Patients

Study of oxidative stress in relation with antioxidant status in chronic bronchitis

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