Muscle and blood redox status after exercise training in severe COPD patients

Rodríguez, Diego A.; Kalko, Susana G.; Puig-Vilanova, Ester; Pérez-Olabarría, Maitane; Falciani, Francesco; Gea, Joaquim; Cascante, Marta; Barreiro, Esther; Roca, Josep

doi:10.1016/j.freeradbiomed.2011.09.022

Cited by 91 publications

(124 citation statements)

References 35 publications

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“…However, the current PR program failed to show the upregulation of antioxidant enzymes in erythrocytes. These observations were consistent with several studies showing that antioxidants enzymes (SOD and CAT) activities were not increased after exercise training in the muscles of COPD patients (Barreiro et al 2009;Rodriguez et al 2012). One possible explanation for the lack of induction of antioxidants in erythrocyte after PR is that the duration of PR used in this study may be shorter than the life span of an erythrocyte in the circulation (90 to 120 days).…”

Section: Discussionsupporting

confidence: 93%

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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Section: Discussionsupporting

confidence: 93%

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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“…Furthermore, in LC-COPD patients, the heaviest smokers were, indeed, those showing the decrease in catalase levels in the tumor lesions compared with the nontumor lungs. These findings are studies in which several markers of oxidative stress were also shown to be increased in patients with only COPD (23,35,46). Moreover, in other studies (10,15,23), patients with LC also exhibited a rise in systemic protein oxidation oxidative stress markers were observed between them, suggesting that the rise in protein oxidation and nitration along with superoxide anion was rather associated with underlying COPD.…”

Section: Discussionsupporting

confidence: 56%

“…Plasma from all individuals was used in this assay (Nitrotyrosine ELISA, Cell Biolabs Inc.) following the manufacturer's instructions and previous studies (23,35).…”

Section: Study Design and Patientsmentioning

confidence: 99%

Redox Imbalance in Lung Cancer of Patients with Underlying Chronic Respiratory Conditions

Mateu-Jiménez

Sánchez-Font

Rodríguez-Fuster

et al. 2016

Mol Med

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Chronic respiratory diseases such as obstructive pulmonary disease (COPD) and oxidative stress may underlie lung cancer (LC). We hypothesized that the profile of oxidative and antioxidant events may differ in lung tumors and blood compartments of patients with non-small cell LC (NSCLC) with and without COPD. Redox markers (immunoblotting, ELISA, chemiluminescence, 2D electrophoresis and proteomics) were analyzed in blood samples of 17 control subjects and 80 LC patients (59 LC-COPD and 21 LC) and lung specimens (tumor and nontumor) from those undergoing thoracotomy (35 patients: 23 LC-COPD and 12 LC). As smoking history was more prevalent in LC-COPD patients, these were further analyzed post hoc as heavy and moderate smokers (cutoff, 60 pack-years). Malondialdehyde (MDA)-protein adducts and SOD1 levels were higher in tumor and nontumor samples of LC-COPD than in LC. In tumors compared with nontumors, SOD2 protein content was greater, whereas catalase levels were decreased in both LC and LC-COPD patients. Blood superoxide anion levels, protein carbonylation and nitration were greater in LC and LC-COPD patients than in the controls, and in the latter patients compared with the former. Systemic superoxide anion, protein carbonyls and nitrotyrosine above specific cutoff values best identified underlying COPD among all patients. Smoking did not influence the study results. A differential expression profile of oxidative stress markers exists in blood and, to a lesser extent, in the tumors of LC-COPD patients. These findings suggest that systemic oxidative stress and lung antioxidants (potential biomarkers) may predispose patients with chronic respiratory diseases to a higher risk for LC.

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“…Their findings of increased Cu-Zn-SOD (mainly located in the cytosol) and decreased Mn-SOD (mainly localized in mitochondria) in atrophied muscle may reflect increased generation of superoxide anions in the cytoplasm rather than the mitochondria, and increased activity of superoxidegenerating XO also supports this possibility. Indeed, oxidative stress has been found not only in the lungs but also in the blood and muscles of stable COPD patients [58][59][60] . For example, there is a negative correlation between the level of oxidative stress within the muscle tissue and muscle strength 58) .…”

Section: Skeletal Muscle Dysfunction and Oxidative Stress In Copdmentioning

confidence: 99%

“…For example, there is a negative correlation between the level of oxidative stress within the muscle tissue and muscle strength 58) . Barreiro et al 60) reported that the levels of lipid peroxidation (4-hydroxy-2-nonenal [HNE] formation) and 3-nitrotyrosine (indicating the generation of peroxynitrite formed by the reaction of superoxide and nitric oxide) were elevated in muscles of COPD patients compared with that in control subjects. This finding suggests that both oxidative and nitrosative stress (O&NS) exists in the quadriceps of COPD patients resulting in muscle dysfunction.…”

Section: Skeletal Muscle Dysfunction and Oxidative Stress In Copdmentioning

confidence: 99%

Skeletal muscle dysfunction and oxidative stress in patients with chronic obstructive lung disease

Oh‐ishi

Nemoto

Saito

2015

JPFSM

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Chronic obstructive pulmonary disease (COPD) is an increasingly important global health problem, including Japan. COPD is associated with an enhanced inflammatory response to irritants in the airways and lungs, in particular cigarette smoke. Cigarette smoke contains gaseous and particulate oxidants, and is considered to be the major etiological factor in the development of COPD. The oxidants in cigarette smoke induce inflammation, and chronic inflammation causes narrowing of the small airways and destruction of the lung parenchyma. Inflammation and oxidative stress are intricately related and seem to play a critical role in the development and/or progression of COPD. There is growing evidence that systemic inflammation exists in patients with stable COPD, leading to extra-pulmonary manifestations including skeletal muscle dysfunction and other comorbidities. Oxidative stress is also observed in skeletal muscle of COPD patients. Therefore, both systemic inflammation and oxidative stress may be associated with skeletal muscle dysfunction in COPD patients, resulting in reduced limb muscle strength and exercise endurance and poor health status and quality of life. Pulmonary rehabilitation is important to improve exercise capacity and health-related quality of life for COPD patients. However, physical exercise, the main component of pulmonary rehabilitation, may increase oxidative stress in the skeletal muscle of such patients. Therefore, rehabilitation programs that not only improve exercise capacity and quality of life, but also reduce exerciseinduced oxidative stress should be established in the future.

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Muscle and blood redox status after exercise training in severe COPD patients

Cited by 91 publications

References 35 publications

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

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

Redox Imbalance in Lung Cancer of Patients with Underlying Chronic Respiratory Conditions

Skeletal muscle dysfunction and oxidative stress in patients with chronic obstructive lung disease

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