Oxidative stress and inflammation in the normal airways and blood of patients with lung cancer and COPD

Barreiro, Esther; Fermoselle, Clara; Mateu-Jiménez, Mercè; Sánchez-Font, Albert; Pijuán, Lara; Gea, Joaquim; Curull, Víctor

doi:10.1016/j.freeradbiomed.2013.08.006

Cited by 76 publications

(98 citation statements)

References 49 publications

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“…In a previous study from our group (25), protein carbonylation levels, as measured by malondialdehyde (MDA)-protein adducts, were also increased in the normal epithelium of patients with LC, especially in patients with underlying COPD, whose levels were significantly greater than in those without this disease. These findings were consistent with those reported in previous investigations, in which a rise in different redox markers was demonstrated in lung tissues or blood of patients with LC (19,20,25,37,101).…”

Section: Redox Balancementioning

confidence: 85%

“…Oxidative stress, defined as the imbalance between oxidants and antioxidants in favor of the former, represents another relevant contributing factor to LC progression (18)(19)(20)(21)(22)(25)(26)(27)(28)33,36) ( Figure 3). Oxidative and nitrosative stress were shown to favor carcinogenesis through the activation of cellular processes that result in neoplastic transformation, the induction of DNA mutations (32,114), or even through induction of macrophage dysfunction (alterations in phagocytosis) (27).…”

Section: Redox Balancementioning

confidence: 99%

“…The study of the underlying biological mechanisms that may predispose patients with chronic respiratory diseases to a higher incidence of LC has also gained much attention in the last few years by several investigators including those listed in this review (25)(26)(27)(28)(29)(30)(31). For instance, oxidative and nitrosative stress as a result of reactive oxygen and nitrogen species (ROS and RNS, respectively) were shown to favor carcinogenesis through the activation of cellular processes that result in neoplastic transformation or the induction of DNA mutations (32).…”

Section: Introductionmentioning

confidence: 99%

“…For instance, oxidative and nitrosative stress as a result of reactive oxygen and nitrogen species (ROS and RNS, respectively) were shown to favor carcinogenesis through the activation of cellular processes that result in neoplastic transformation or the induction of DNA mutations (32). Other investigations have also demonstrated the contribution of oxidative damage, inflammatory events, and tumor microenvironment to lung carcinogenesis in patients and animal models (19,20,(25)(26)(27)(28)(29)(30)(31)(33)(34)(35)(36)(37).…”

Section: Introductionmentioning

confidence: 99%

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Relationships between chronic obstructive pulmonary disease and lung cancer: biological insights

Barreiro¹,

Bustamante

Curull³

et al. 2016

J. Thorac. Dis.

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Lung cancer (LC) has become one of the leading causes of preventable death in the last few decades. Cigarette smoking (CS) stays as the main etiologic factor of LC despite that many other causes such as occupational exposures, air pollution, asbestos, or radiation have also been implicated. Patients with chronic obstructive pulmonary disease (COPD), which also represents a major cause of morbidity and mortality in developed countries, exhibit a significantly greater risk of LC. The study of the underlying biological mechanisms that may predispose patients with chronic respiratory diseases to a higher incidence of LC has also gained much attention in the last few years. The present review has been divided into three major sections in which different aspects have been addressed: (I) relevant etiologic agents of LC; (II) studies confirming the hypothesis that COPD patients are exposed to a greater risk of developing LC; and (III) evidence on the most relevant underlying biological mechanisms that support the links between COPD and LC. Several carcinogenic agents have been described in the last decades but CS remains to be the leading etiologic agent in most geographical regions in which the incidence of LC is very high. Growing evidence has put the line forward the implications of COPD and especially of emphysema in LC development. Hence, COPD represents a major risk factor of LC in patients. Different avenues of research have demonstrated the presence of relevant biological mechanisms that may predispose COPD patients to develop LC. Importantly, the so far identified biological mechanisms offer targets for the design of specific therapeutic strategies that will further the current treatment options for patients with LC. Prospective screening studies, in which patients with COPD should be followed up for several years will help identify biomarkers that may predict the risk of LC among these patients.

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Section: Redox Balancementioning

confidence: 85%

Section: Redox Balancementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Relationships between chronic obstructive pulmonary disease and lung cancer: biological insights

Barreiro¹,

Bustamante

Curull³

et al. 2016

J. Thorac. Dis.

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“…In fact, when this homeostasis is disrupted and there are more reactive species than antioxidants several diseases can develop. 15 Recent studies indicate that an increased oxidative stress is related to the pathogenesis of COPD, 1,[16][17][18] and contribute this to the fact that COPD patients produce more H 2 O 2 compared to "healthy". 19 Another study hypothesized that loss of asthmatic SOD activity is due to greater susceptibility to oxidative inactivation.…”

Section: Discussionmentioning

confidence: 99%

Role of Apo E and superoxide dismutase in patients with obstructive lung diseases

Almzaiel

Al-Ameri

Tariq

2017

J. contemp. med. sci.

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Objective Obstructive lung diseases (OLD) are chronic inflammatory disorders of the respiratory tract including asthma and chronic obstructive pulmonary disease (COPD). Apo lipoprotein E (Apo E), is a multifunctional protein as it intervenes the binding of lipoproteins or lipid complexes to specific cell-surface receptors. Experimental studies referred to the function of Apo E as an endogenous negative regulator of airway hyper responsiveness and goblet cell hyperplasia. The protective role of Apo E pathways primarily in respiratory disease was explained in human studies and research utilizing experimental murine model systems. Literature data reveal a strong association between redox status, including the enzyme superoxide dismutase (SOD) with both the development a severity of OLD. This study aims to investigate the relation between SOD antioxidant enzyme activity in addition to investigating the level of Apo E and the development of obstructive lung diseases (OLD). Methods Patients with OLD (n = 40) and 40 age-matched healthy controls were enrolled in this study. Serum samples were collected to test the role of Apo E and to test the effect of antioxidant enzyme SOD, and their influence on OLD, all measured by ELISA.Result The results showed a significant decrease in the level of serum SOD activity in patients with OLD when compared with control group (P < 0.05). However, the levels of Apo E did not show a significant difference between the two groups. Conclusion Decreased level of antioxidant SOD suggests the presence of an oxidative stress in asthmatic airways favoring a more oxidative state is present in the airway inflammation. The level of Apo E was non significantly increased in serum of patient, this suggests that protein level of Apo E does not change but may be Apo E gene expression is altered.

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Chronic Obstructive Pulmonary Disease and Oxidative Damage

Barreiro

2017

Protein Carbonylation

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Oxidative stress and inflammation in the normal airways and blood of patients with lung cancer and COPD

Cited by 76 publications

References 49 publications

Relationships between chronic obstructive pulmonary disease and lung cancer: biological insights

Relationships between chronic obstructive pulmonary disease and lung cancer: biological insights

Role of Apo E and superoxide dismutase in patients with obstructive lung diseases

Chronic Obstructive Pulmonary Disease and Oxidative Damage

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