Altered antioxidant enzyme activity with severity and comorbidities of chronic obstructive pulmonary disease (COPD) in South Indian population

Asimuddin, Mohammed; Gutta, Vijayalakshmi; Ansari, Mohd Soheb; Venkata, Rajagopal Saladi; Jamil, Kaiser

doi:10.1186/s40749-017-0023-z

Cited by 10 publications

(10 citation statements)

References 54 publications

(58 reference statements)

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“…Our findings are consistent with clinical data; a study reported reduced GPx activity in smokers with COPD compared to healthy controls (smokers or non-smokers) [34]. GPx activity was also lower in COPD patients compared to healthy controls [35], in severe COPD compared to moderate disease [35, 36], and in moderate COPD compared to mild disease [35, 37]. Moreover, Golpon et al reported downregulation of the GPX3 gene in patients with severe emphysema [38].…”

Section: Discussionsupporting

confidence: 91%

Role of GPx3 in PPARγ-induced protection against COPD-associated oxidative stress

Reddy

Lakshmi

Banno

et al. 2018

Free Radical Biology and Medicine

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Cigarette smoke, a source of numerous oxidants, produces oxidative stress and exaggerated inflammatory responses that lead to irreversible lung tissue damage. It is the single, most significant risk factor for chronic obstructive pulmonary disease (COPD). Although an intrinsic defense system that includes both enzymatic and non-enzymatic modulators exists to protect lung tissues against oxidative stress, impairment of these protective mechanisms has been demonstrated in smokers and COPD patients. The antioxidant enzyme GSH peroxidase (GPx) is an important part of this intrinsic defense system. Although cigarette smoke has been shown to downregulate its expression and activity, the underlying mechanism is not known. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear hormone receptor with antioxidant effects. PPARγ activation has demonstrated protective effects against cigarette smoke-induced oxidative stress and inflammation. Molecular mechanisms for PPARγ's antioxidant function likewise remain to be elucidated. This study explored the link between PPARγ and GPx3 and found a positive association in cigarette smoke extract (CSE)-exposed human bronchial epithelial cells. Moreover, we provide evidence that identifies GPx3 as a PPARγ transcriptional target. Attenuation of antioxidant effects in the absence of GPx3 highlights the antioxidant's prominent role in mediating PPARγ's function. We also demonstrate that ligand-mediated PPARγ activation blocks CSE-induced reactive oxygen species and hydrogen peroxide production via upregulation of GPx3. In summary, our findings describing the molecular mechanisms involving GPx3 and PPARγ in CSE-induced oxidative stress and inflammation may provide valuable information for the development of more effective therapeutics for COPD.

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Section: Discussionsupporting

confidence: 91%

Role of GPx3 in PPARγ-induced protection against COPD-associated oxidative stress

Reddy

Lakshmi

Banno

et al. 2018

Free Radical Biology and Medicine

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“…Glutathione (GSH), an antioxidant in the epithelial lining fluid [99], is an essential intermediate in the conversion of hydrogen peroxide to water and lipid peroxides degradation [100]. In addition, GSH might improve inflammation by inhibiting NF-κB activation.…”

Section: The Role Of Metabolism Dysfunction In Copd Pathogenesismentioning

confidence: 99%

An Updated Overview of Metabolomic Profile Changes in Chronic Obstructive Pulmonary Disease

Ran

Pang

et al. 2019

Metabolites

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Chronic obstructive pulmonary disease (COPD), a common and heterogeneous respiratory disease, is characterized by persistent and incompletely reversible airflow limitation. Metabolomics is applied to analyze the difference of metabolic profile based on the low-molecular-weight metabolites (<1 kDa). Emerging metabolomic analysis may provide insights into the pathogenesis and diagnosis of COPD. This review aims to summarize the alteration of metabolites in blood/serum/plasma, urine, exhaled breath condensate, lung tissue samples, etc. from COPD individuals, thereby uncovering the potential pathogenesis of COPD according to the perturbed metabolic pathways. Metabolomic researches have indicated that the dysfunctions of amino acid metabolism, lipid metabolism, energy production pathways, and the imbalance of oxidations and antioxidations might lead to local and systematic inflammation by activating the Nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway and releasing inflammatory cytokines, like interleutin-6 (IL-6), tumor necrosis factor-α, and IL-8. In addition, they might cause protein malnutrition and oxidative stress and contribute to the development and exacerbation of COPD.

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“…Of these, 13 were further excluded, either because of missing information or they did not fulfil the inclusion criteria. Finally, 24 studies were included in the meta-analysis [ 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 ]. A total of 2214 COPD patients (mean age 60 years, 74% male), and 1608 non-COPD subjects (mean age 55 years, 71% male) were evaluated.…”

Section: Resultsmentioning

confidence: 99%

“…Fifteen studies on 1329 COPD patients (mean age 60 years, 79% male) and 814 non-COPD subjects (mean age 54 years, 71% male) were identified [ 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ]. COPD was diagnosed according to the Global Obstructive Lung Disease (GOLD) guidelines in 12 studies [ 25 , 26 , 28 , 29 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 ], and the American Thoracic Society/European Respiratory Society (ATS/ERS) guidelines in three [ 27 , 30 , 39 ]. Thirteen studies assessed erythrocytes [ 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 37 , 39 ] whereas the remaining two assessed whole blood [ 36 , 38 ].…”

Section: Resultsmentioning

confidence: 99%

Glutathione Peroxidase in Stable Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-analysis

Zinellu¹,

Zinellu

Pau

et al. 2021

Antioxidants

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Chronic obstructive pulmonary disease (COPD) is a progressive disease that is characterized by a state of persistent inflammation and oxidative stress. The presence of oxidative stress in COPD is the result of an imbalance between pro-oxidant and antioxidant mechanisms. The aim of this review was to investigate a possible association between glutathione peroxidase (GPx), a key component of antioxidant defense mechanisms, and COPD. A systematic search for relevant studies was conducted in the electronic databases PubMed, Web of Science, Scopus, and Google Scholar, from inception to June 2021. Standardized mean differences (SMDs) were used to express the differences in GPx concentrations between COPD patients and non-COPD subjects. Twenty-four studies were identified. In 15 studies assessing whole blood/erythrocytes (GPx isoform 1), the pooled results showed that GPx concentrations were significantly lower in patients with COPD (SMD = −1.91, 95% CI −2.55 to −1.28, p < 0.001; moderate certainty of evidence). By contrast, in 10 studies assessing serum/plasma (GPx isoform 3), the pooled results showed that GPx concentrations were not significantly different between the two groups (very low certainty of evidence). The concentration of GPx-1, but not GPx-3, is significantly lower in COPD patients, suggesting an impairment of antioxidant defense mechanisms in this group.

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Altered antioxidant enzyme activity with severity and comorbidities of chronic obstructive pulmonary disease (COPD) in South Indian population

Cited by 10 publications

References 54 publications

Role of GPx3 in PPARγ-induced protection against COPD-associated oxidative stress

Role of GPx3 in PPARγ-induced protection against COPD-associated oxidative stress

An Updated Overview of Metabolomic Profile Changes in Chronic Obstructive Pulmonary Disease

Glutathione Peroxidase in Stable Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-analysis

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