Effects of Cigarette Smoke on Oxidant-Antioxidant System of Lung Tissue

2021 ◽  
pp. 1-15
Author(s):  
Hikmet Can Çubukçu ◽  
İlker Durak
Keyword(s):  
Cigarette Smoke ◽  
Antioxidant System ◽  
Lung Tissue

scholarly journals Cigarette smoke alters the transcriptome of non-involved lung tissue in lung adenocarcinoma patients

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Giulia Pintarelli ◽  
Sara Noci ◽  
Davide Maspero ◽  
Angela Pettinicchio ◽  
Matteo Dugo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Adenocarcinoma ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Gene Networks ◽  
Lung Parenchyma ◽  
Fold Change ◽  
Differentially Expressed ◽  
Significant Gene ◽  
Never Smokers

Abstract Alterations in the gene expression of organs in contact with the environment may signal exposure to toxins. To identify genes in lung tissue whose expression levels are altered by cigarette smoking, we compared the transcriptomes of lung tissue between 118 ever smokers and 58 never smokers. In all cases, the tissue studied was non-involved lung tissue obtained at lobectomy from patients with lung adenocarcinoma. Of the 17,097 genes analyzed, 357 were differentially expressed between ever smokers and never smokers (FDR < 0.05), including 290 genes that were up-regulated and 67 down-regulated in ever smokers. For 85 genes, the absolute value of the fold change was ≥2. The gene with the smallest FDR was MYO1A (FDR = 6.9 × 10−4) while the gene with the largest difference between groups was FGG (fold change = 31.60). Overall, 100 of the genes identified in this study (38.6%) had previously been found to associate with smoking in at least one of four previously reported datasets of non-involved lung tissue. Seven genes (KMO, CD1A, SPINK5, TREM2, CYBB, DNASE2B, FGG) were differentially expressed between ever and never smokers in all five datasets, with concordant higher expression in ever smokers. Smoking-induced up-regulation of six of these genes was also observed in a transcription dataset from lung tissue of non-cancer patients. Among the three most significant gene networks, two are involved in immunity and inflammation and one in cell death. Overall, this study shows that the lung parenchyma transcriptome of smokers has altered gene expression and that these alterations are reproducible in different series of smokers across countries. Moreover, this study identified a seven-gene panel that reflects lung tissue exposure to cigarette smoke.

scholarly journals AP-2α expression and cell apoptosis of the lung tissue of rats with COPD and ECV304 cells stimulated by cigarette smoke extract

2011 ◽  
Vol 56 (15) ◽  
pp. 1562-1568 ◽  
Author(s):  
JunLi Li ◽  
Yan Chen ◽  
Ping Chen ◽  
Shan Cai ◽  
Hong Peng ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cell Apoptosis ◽  
Cigarette Smoke Extract

Humic-like substances in cigarette smoke condensate and lung tissue of smokers

1994 ◽  
Vol 266 (4) ◽  
pp. L382-L388 ◽  
Author(s):  
A. J. Ghio ◽  
J. Stonehuerner ◽  
D. R. Quigley
Keyword(s):  
Free Radical ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cigarette Smoke Exposure ◽  
Cigarette Smoke Condensate ◽  
Free Radical Generation ◽  
Carboxylate Content ◽  
Radical Generation

Deposition of pigmented matter in the lower respiratory tract correlates with the extent of emphysema in smokers as well as with free radical generation and iron accumulation. Pulmonary emphysema is postulated to be mediated by free radical generation which is either directly or indirectly associated with cigarette smoke exposure. The hypothesis was tested that 1) incomplete combustion of tobacco yields humic-like substances (HLS) which 2) deposit in the lung as pigmented particulates, 3) complex iron cations in vitro and in vivo, and 4) have a capacity to catalyze oxidant formation. HLS, isolated by alkali extraction of cigarette smoke condensate (CSC) (Tobacco Health Research Institute, University of Kentucky), demonstrated a high carbon and low carboxylate content on elemental and functional group analyses, respectively, compared with values for HLS sequestered from soils. The HLS isolated from CSC had a capacity to complex iron in vitro and accumulated the metal in vivo after intratracheal instillation in an animal model. Both HLS and its iron complex generated free radicals, and some portion of this oxidant generation was metal dependent. Lung tissue collected at autopsy from smokers contained HLS with an infrared spectrum almost identical to that of the material isolated from CSC. Associations between particulate deposition, metal accumulation, and free radical generation suggest a possible role of HLS in the induction of lung disease following cigarette exposure.

scholarly journals The time pattern of selenomethionine administration in preventing free radicals due to exposure to electric cigarette smoke

2021 ◽  
Vol 10 (2) ◽  
Author(s):  
Rivan Virlando Suryadinata ◽  
Bambang Wirjatmadi ◽  
Amelia Lorensia
Keyword(s):  
Free Radicals ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cell Damage ◽  
Control Group ◽  
Early Application ◽  
Control Group Design ◽  
Time Pattern ◽  
Negative Effect ◽  
Male Wistar Rats

Background: Most people believe that electric cigarettes have no negative effect on health,  which causes them to use it more. However, exposure to the smoke from these cigarettes is bad for the health and causes cell damage. Antioxidants play an important role in preventing cell damage, and they can be obtained through the oral administration of selenomethionine.Design and methods: This study used an experimental method and a post-test control group design. Male Wistar rats, which were exposed to cigarette smoke were given selenomethionine orally and then tested for the presence of free radicals. The measurement of lung tissue damage was conducted by assessing the level of malondialdehyde in the blood and immunohistochemistry (IHC) of the lung tissue.Result: The study showed that differences in the time of administration of selenomethionine affect the levels of malondialdehyde in the blood and expression of malondialdehyde in the lung tissue (p<0.05). Consequently, the two groups showed a strong (r=0.861) and significant (p=0.000) relationship with each other.Conclusion: The early application of selenomethionine can prevent increased levels of malondialdehyde in the blood and lung tissue due to exposure to e-cigarette smoke.

scholarly journals From blood to lung tissue: effect of cigarette smoke on DNA methylation and lung function

2018 ◽  
Vol 19 (1) ◽  
Author(s):  
Maaike de Vries ◽  
Diana A van der Plaat ◽  
Ivana Nedeljkovic ◽  
Rikst Nynke Verkaik-Schakel ◽  
Wierd Kooistra ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Lung Function ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Tissue Effect

Polyphenols from Juglans regia L. (walnut) kernel modulate cigarette smoke extract induced acute inflammation, oxidative stress and lung injury in Wistar rats

2010 ◽  
Vol 30 (6) ◽  
pp. 499-506 ◽  
Author(s):  
Wajhul Qamar ◽  
Sarwat Sultana
Keyword(s):  
Lung Injury ◽  
Cell Count ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Total Protein ◽  
Wistar Rats ◽  
Juglans Regia ◽  
Cigarette Smoke Extract ◽  
Total Cell ◽  
Total Cell Count

The present study was designed to evaluate the protective effects of Juglans regia kernel extract against cigarette smoke extract (CSE)-induced lung toxicities in Wistar rats. Prophylactic treatment of methanolic extract of J. regia kernel at the doses of 50 mg/kg b.wt. and 100 mg/kg b.wt was given by gavage to Wistar rats for 1 week prior to CSE exposure. Female Wistar rats were administered with single dose (1.3 mL/kg b.wt.) of CSE through intratracheal instillation. Lung injury markers lactate dehydrogenase (LDH) activity, total cell count, total protein and reduced glutathione (GSH) in bronchoalveolar lavage fluid (BALF) were evaluated. Glutathione reductase (GR), xanthine oxidase (XO) and catalase activities were measured in lung tissue. J. regia extract significantly decreased the levels of LDH, total cell count, total protein and increased the GSH level in BALF, it also significantly restored the levels of GR, catalase and reduced the XO activity in lung tissue. Total polyphenolic content of J. regia kernel extract was found to be 96 ± 0.81 mg gallic acid equivalent (GAE)/g dry weight of extract. In DPPH (2,2-Diphenyl-1-Picrylhydrazyl) assay, the extract shows high free radical scavenging potential. On the basis of these results, protective role of J. regia extract against CSE-induced acute lung toxicity in Wistar rats is suggested.

scholarly journals p19Arf Exacerbates Cigarette Smoke-Induced Pulmonary Dysfunction

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 462
Author(s):  
Ryuta Mikawa ◽  
Tadashi Sato ◽  
Yohei Suzuki ◽  
Hario Baskoro ◽  
Koichiro Kawaguchi ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Cellular Senescence ◽  
Cigarette Smoke Extract ◽  
Senescent Cell ◽  
Cigarette Smoke Exposure ◽  
Pulmonary Dysfunction ◽  
Potential Therapeutic Target ◽  
Tissue Compliance

Senescent cells accumulate in tissues during aging or pathological settings. The semi-genetic or pharmacological targeting of senescent cells revealed that cellular senescence underlies many aspects of the aging-associated phenotype and diseases. We previously reported that cellular senescence contributes to aging- and disease-associated pulmonary dysfunction. We herein report that the elimination of Arf-expressing cells ameliorates cigarette smoke-induced lung pathologies in mice. Cigarette smoke induced the expression of Ink4a and Arf in lung tissue with concomitant increases in lung tissue compliance and alveolar airspace. The elimination of Arf-expressing cells prior to cigarette smoke exposure protected against these changes. Furthermore, the administration of cigarette smoke extract lead to pulmonary dysfunction, which was ameliorated by subsequent senescent cell elimination. Collectively, these results suggest that senescent cells are a potential therapeutic target for cigarette smoking-associated lung disease.

The Effects of Naringin on Cigarette Smoke-Induced Dynamic Changes in Oxidation/Antioxidant System in Lung of Mice

2020 ◽  
Vol 15 (8) ◽  
pp. 1934578X2094723
Author(s):  
Pan Chen ◽  
Ziting Xiao ◽  
Hao Wu ◽  
Yonggang Wang ◽  
Weiwei Su ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Cigarette Smoke ◽  
Antioxidant System ◽  
Antioxidant Systems ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dynamic Changes ◽  
Tnf Α ◽  
Nrf2 Signaling Pathway

Naringin possesses strong antioxidative activity and can protect against some respiratory diseases. Oxidative stress is thought to be a major factor in the development of many tobacco-caused diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway plays a critical role in the regulation of oxidative stress. The dynamic changes in the antioxidant system in the lung that are induced by cigarette smoke (CS) are not well investigated, and how naringin affects these changes remains unknown. This study aimed to investigate the dynamic changes between the oxidation and antioxidant systems resulting from CS exposure and the effects of naringin on these changes in mice. Mice were chronically exposed to CS for 30 days. The levels of malondialdehyde (MDA), glutathione (GSH), interleukin (IL)-6, and tumor necrosis factor-alpha (TNF-α); the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); and the expressions of Nrf2, heme oxygenase-1 (HO-1), and nicotinamide adenine dinucleotide phosphate quinone dehydrogenase 1 (NQO1) in lung tissue were measured on days 2, 7, and 30. The levels of MDA, GSH, IL-6, and TNF-α in the lung were found to increase throughout the exposure. SOD and GSH-Px activities showed an increase on day 2 and a decrease on days 7 and 30. The messenger ribonucleic acid expressions of Nrf2, HO-1, and NQO1 were elevated on day 2 and decreased on day 7; Nrf2 and HO-1 expressions were continually decreased, but NQO1 expression was increased again, on day 30. Naringin restored the levels of these biochemical indices to normal throughout the experiment, suggesting that naringin protected against the CS-induced oxidative damage by suppressing the increase of antioxidants resulting from the early stage of CS exposure, as well as inhibiting the depletion of antioxidants due to long-term oxidative stress. Naringin also suppressed lung inflammation by inhibiting IL-6 and TNF-α. These results indicate that naringin possesses a powerful ability to maintain the balance of the oxidation/antioxidant system in the lung when subjected to CS exposure, probably by regulating the Nrf2 signaling pathway.

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