Oxidative Stress in COPD Patients, Smokers, and Non-smokers

Tavilani, Heidar; Nadi, Ebrahim; Karimi, Jamshid; Goodarzi, Mohammad Taghi

doi:10.4187/respcare.01809

Cited by 56 publications

(64 citation statements)

References 23 publications

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“…Our results demonstrated sufficiently Mean difference (COPD group minus control group) is expressed as mean Ϯ SE. SPD ϭ surfactant protein D decreased levels of serum superoxide dismutase 3 in the COPD group compared with the control group and are in agreement with those of Zeng et al, 50 Gavali et al, 51 and Tavilani et al 52 This decreased activity in subjects with COPD probably results from an increase in consumption of antioxidants. 53 We found a superoxide dismutase 3 levels of 244.79 Ϯ 69.12 U/L in the control group (see Table 4), whereas Chakraborty et al 54 reported plasma superoxide dismutase levels of 4.06 Ϯ 0.26 U/mL, KoturStevuljevic et al 55 found plasma superoxide dismutase levels of 153 Ϯ 36 U/L in non-coronary heart disease control subjects, and Comhair et al 56 reported a mean serum superoxide dismutase level of 2.75 U/mL.…”

Section: Discussionsupporting

confidence: 89%

Diagnostic Utility of Biomarkers in COPD

Ambade¹,

Sontakke

Barthwal³

et al. 2015

Respir Care

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BACKGROUND: COPD will become the third leading cause of death by 2020. There are many situations in which spirometry, the primary tool for diagnosis of COPD, cannot be performed, and thus, the staging and status of these patients cannot be determined. To date, there is no known biochemical marker used for diagnosing COPD. This study aimed to explore the utility of biomarkers for diagnosis of COPD. METHODS: This was an observational study composed of 96 stable subjects with COPD and 96 subjects with normal lung function. Each group contained an equal number of smokers and nonsmokers. Serum levels of superoxide dismutase 3, glutathione peroxidase, catalase, ceruloplasmin ferroxidase activity, C-reactive protein, and surfactant protein D (SPD) were estimated. Ferroxidase activity was estimated by a kinetic method, whereas the other analytes were measured by enzyme-linked immunosorbent assay. The cutoff value, sensitivity and specificity at the cutoff value, and area under the curve for each analyte were determined from receiver operating characteristic curve. RESULTS: Significantly decreased superoxide dismutase 3 and increased ferroxidase activity, SPD, glutathione peroxidase, and C-reactive protein levels were found in subjects with COPD. For all subjects and nonsmoking subjects with COPD, the area under the curve was highest for ferroxidase activity, followed by glutathione peroxidase, SPD, and C-reactive protein, with a sensitivity and specificity of > 73%. For smoking subjects with COPD, the area under the curve was highest for SPD, followed by glutathione peroxidase, ferroxidase activity, and C-reactive protein, with a sensitivity and specificity > 67%. Some combinations of markers were found to give either a sensitivity or specificity of > 95%, which can be utilized to rule in and rule out COPD. CONCLUSIONS: Biomarkers can be reliably utilized in the diagnosis of COPD. Of all the markers, SPD appears to be the most promising in smokers, whereas ferroxidase activity shows promise in nonsmokers. To rule out COPD, ferroxidase activity or glutathione peroxidase can be potentially useful, whereas to rule in COPD, ferroxidase activity and glutathione peroxidase appear to be the most promising combination in both nonsmoking and smoking subjects.

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Section: Discussionsupporting

confidence: 89%

Diagnostic Utility of Biomarkers in COPD

Ambade¹,

Sontakke

Barthwal³

et al. 2015

Respir Care

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“…The mRNA expressions of Mn-SOD and Cu Zn-SOD were significantly increased in the lungs of SM-exposed patients [27]. SOD, CAT and GST activities may be increased or decreased in various pulmonary diseases including asthma and COPD [6,11,17,25]. Jafari and Ghanei reported a significant increase in SOD and CAT activities in plasma, erythrocytes, and brochoalveolar lavage fluid (BAL) and GST activity in BAL of patients with SM-induced lung injuries [8].…”

Section: Discussionmentioning

confidence: 99%

“…Volume 11, No 5, September-October2017; http://www.ijt.ir dismutase (SOD), catalase (CAT), glutathione Stransferase (GST) and large amounts of glutathione (GSH) [11]. SM-induced oxidative stress is associated with alteration of antioxidant enzyme activities, depletion of GSH and an increase of membrane lipid peroxidation in tissues, all of which can lead to inflammation and ultimately induction of cell death [9,[12][13][14].…”

Section: Introductionmentioning

confidence: 99%

The Role of Oxidative Stress in Severity of Obstructive Pulmonary Complications in Sputum of Sulfur Mustard-Injured Patients

Heydari

Jafari

Khazaie

et al. 2017

IJT

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“…Mak et al (25) showed that erythrocyte catalase activity increased in patients with COPD, which is different from our findings. However, Tavilani et al (26) and some others demonstrated that antioxidant enzyme might be downregulated during severe or chronic oxidant exposure (27). CAPE incubation significantly restored catalase activity in this study.…”

Section: Discussionmentioning

confidence: 99%

Caffeic acid phenethyl ester protects lung alveolar epithelial cellsfrom cigarette smoke-induced damage

Barlas¹,

Erdoğan²

2015

Turk J Med Sci

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Background/aim: To evaluate the influence of caffeic acid phenethyl ester (CAPE) on cigarette smoke (CS)-induced cell damage, oxidative stress, and inflammation in human alveolar epithelial cells.Materials and methods: A549 alveolar epithelial cells were divided into control, CS exposure, CAPE, and CS+CAPE treatment groups. Undiluted CS-exposed medium (100%) and three dilutions (50%, 25%, and 10%) of CS-exposed media were applied to cultured A549 cells, which were analyzed after 3 h of incubation. Viability was measured by MTT assay, the gene expressions were evaluated by realtime PCR, and spectrophotometric techniques were used for biochemical assessments.Results: While CS exposure markedly reduced cellular viability by 32% after 3 h of incubation, 2.5 µM CAPE treatments prevented CSinduced cell death by 40% in the cells. CS exposure triggered lipid peroxidation and depleted antioxidant capacity through inhibiting catalase activity and depleting glutathione levels. Moreover, CS increased nitric oxide production via upregulation of iNOS expression. CAPE treatment significantly restored antioxidant capacity and prevented lipid peroxidation. Cigarette smoke exposure induced inflammation by significantly upregulating TNF-α, IL-1β, and COX-2 mRNA expressions (3-, 2-and 25-fold, respectively). CAPE treatment of A549 cells significantly reversed the inflammation. Conclusion:CAPE may potentially represent a new therapeutic option in the prevention of CS-induced lung damages.

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Oxidative Stress in COPD Patients, Smokers, and Non-smokers

Abstract: Decreased total antioxidant capacity in plasma of subjects with COPD and smokers suggests an increased oxidative stress in this group. However, no relationship was found between lung function and antioxidant systems status in COPD subjects.

Cited by 56 publications

References 23 publications

Diagnostic Utility of Biomarkers in COPD

Diagnostic Utility of Biomarkers in COPD

The Role of Oxidative Stress in Severity of Obstructive Pulmonary Complications in Sputum of Sulfur Mustard-Injured Patients

Caffeic acid phenethyl ester protects lung alveolar epithelial cellsfrom cigarette smoke-induced damage

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