scholarly journals Glutathione-S-transferase P protects against endothelial dysfunction induced by exposure to tobacco smoke

2009 ◽  
Vol 296 (5) ◽  
pp. H1586-H1597 ◽  
Author(s):  
Daniel J. Conklin ◽  
Petra Haberzettl ◽  
Russell A. Prough ◽  
Aruni Bhatnagar
Keyword(s):  
Endothelial Dysfunction ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Cardiovascular Effects ◽  
Tobacco Smoke Exposure ◽  
Mouse Lung ◽  
Organ Bath ◽  
Systemic Delivery ◽  
Total Plasma Protein ◽  
Risk Of Cancer

Exposure to tobacco smoke impairs endothelium-dependent arterial dilation. Reactive constituents of cigarette smoke are metabolized and detoxified by glutathione- S-transferases (GSTs). Although polymorphisms in GST genes are associated with the risk of cancer in smokers, the role of these enzymes in regulating the cardiovascular effects of smoking has not been studied. The P isoform of GST (GSTP), which catalyzes the conjugation of electrophilic molecules in cigarette smoke such as acrolein, was expressed in high abundance in the mouse lung and aorta. Exposure to tobacco smoke for 3 days (5 h/day) decreased total plasma protein. These changes were exaggerated in GSTP−/− mice. Aortic rings isolated from tobacco smoke-exposed GSTP−/− mice showed greater attenuation of ACh-evoked relaxation than those from GSTP+/+ mice. The lung, plasma, and aorta of mice exposed to tobacco smoke or acrolein (for 5 h) accumulated more acrolein-adducted proteins than those tissues of mice exposed to air, indicating that exposure to tobacco smoke results in the systemic delivery of acrolein. Relative to GSTP+/+ mice, modification of some proteins by acrolein was increased in the aorta of GSTP−/− mice. Aortic rings prepared from GSTP−/− mice that inhaled acrolein (1 ppm, 5 h/day for 3 days) or those exposed to acrolein in an organ bath showed diminished ACh-induced arterial relaxation more strongly than GSTP+/+ mice. Acrolein-induced endothelial dysfunction was prevented by pretreatment of the aorta with N-acetylcysteine. These results indicate that GSTP protects against the endothelial dysfunction induced by tobacco smoke exposure and that this protection may be related to the detoxification of acrolein or other related cigarette smoke constituents.

Comparison of Oxidative Effects of Electronic Cigarette and Tobacco Smoke Exposure Performed Experimentally

2021 ◽  
pp. 1-7
Author(s):  
Oktay Aslaner
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Electronic Cigarette ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Control Group ◽  
Exposure Group ◽  
Oxidative Effects

<b><i>Objective:</i></b> Cigarette smoking is a life-threatening habit that has rapidly spread in every socioeconomic part of the public worldwide. There exist mechanisms of nicotine delivery available to use in the hope of halting cigarette smoking, and the electronic cigarette (EC) is one of the common methods used for tobacco smoking replacement. This study aimed to investigate experimentally the oxidative effects of tobacco smoke and EC smoke which contain nicotine. <b><i>Method:</i></b> We constructed smoke circuit rooms for exposing the rats to EC or tobacco smoke. Three groups were created, the control group (<i>N</i> = 8); the electronic cigarette group (<i>N</i> = 8), exposure to electronic cigarette smoke for 2 h per day; and the tobacco group (<i>N</i> = 8), exposure to traditional cigarette smoke for 2 h per day. After the first and second week of exposure, blood samples were obtained, and serum oxidative stress index (OSI), paraoxonase 1 (PON1) activity, and prolidase levels were evaluated. <b><i>Results:</i></b> Higher values of OSI and prolidase levels were detected in the first week of EC or tobacco smoke exposure in both study groups (<i>p</i> &#x3c; 0.001) when compared with the control group, and partial decrements were observed in the second week. By contrast, elevated PON1 levels were observed in the second week after EC or tobacco smoke exposure. The highest OSI levels were observed in the tobacco smoke group (<i>p</i> &#x3c; 0.001). The lowest values of PON1 levels were detected in the first week of the electronic cigarette smoke group, and this decremental value was statistically different than normal, the second week of the electronic cigarette smoke group, the first week of the traditional cigarette smoke exposure group, and the second week of the traditional cigarette smoke exposure group values (<i>p</i> &#x3c; 0.000). <b><i>Conclusion:</i></b> Our results indicate that EC smoke induced oxidative stress. Therefore, ECs are potentially risky for human health and can lead to important health problems.

scholarly journals Tobacco smoking induces cardiovascular mitochondrial oxidative stress, promotes endothelial dysfunction, and enhances hypertension

2019 ◽  
Vol 316 (3) ◽  
pp. H639-H646 ◽  
Author(s):  
Sergey Dikalov ◽  
Hana Itani ◽  
Bradley Richmond ◽  
Liaison Arslanbaeva ◽  
Aurelia Vergeade ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Tobacco Smoking ◽  
Smoke Exposure ◽  
Metabolic Reprogramming ◽  
Wild Type ◽  
Mitochondrial Oxidative Stress

Tobacco smoking is a major risk factor for cardiovascular disease and hypertension. It is associated with the oxidative stress and induces metabolic reprogramming, altering mitochondrial function. We hypothesized that cigarette smoke induces cardiovascular mitochondrial oxidative stress, which contributes to endothelial dysfunction and hypertension. To test this hypothesis, we studied whether the scavenging of mitochondrial H2O2 in transgenic mice expressing mitochondria-targeted catalase (mCAT) attenuates the development of cigarette smoke/angiotensin II-induced mitochondrial oxidative stress and hypertension compared with wild-type mice. Two weeks of exposure of wild-type mice with cigarette smoke increased systolic blood pressure by 17 mmHg, which was similar to the effect of a subpresssor dose of angiotensin II (0.2 mg·kg−1·day−1), leading to a moderate increase to the prehypertensive level. Cigarette smoke exposure and a low dose of angiotensin II cooperatively induced severe hypertension in wild-type mice, but the scavenging of mitochondrial H2O2 in mCAT mice completely prevented the development of hypertension. Cigarette smoke and angiotensin II cooperatively induced oxidation of cardiolipin (a specific biomarker of mitochondrial oxidative stress) in wild-type mice, which was abolished in mCAT mice. Cigarette smoke and angiotensin II impaired endothelium-dependent relaxation and induced superoxide overproduction, which was diminished in mCAT mice. To mimic the tobacco smoke exposure, we used cigarette smoke condensate, which induced mitochondrial superoxide overproduction and reduced endothelial nitric oxide (a hallmark of endothelial dysfunction in hypertension). Western blot experiments indicated that tobacco smoke and angiotensin II reduce the mitochondrial deacetylase sirtuin-3 level and cause hyperacetylation of a key mitochondrial antioxidant, SOD2, which promotes mitochondrial oxidative stress. NEW & NOTEWORTHY This work demonstrates tobacco smoking-induced mitochondrial oxidative stress, which contributes to endothelial dysfunction and development of hypertension. We suggest that the targeting of mitochondrial oxidative stress can be beneficial for treatment of pathological conditions associated with tobacco smoking, such as endothelial dysfunction, hypertension, and cardiovascular diseases. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/mitochondrial-oxidative-stress-in-smoking-and-hypertension/ .

scholarly journals Household Environmental Tobacco Smoke and Risk of Allergic Sensitization Among Children with Asthma

2013 ◽  
Vol 59 (1) ◽  
pp. 36-39
Author(s):  
Brîndușa Căpîlna ◽  
Maria Despina Baghiu
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Respiratory Infections ◽  
Negative Impact ◽  
Allergic Sensitization ◽  
Specific Ige ◽  
Tobacco Smoke Exposure ◽  
Food Allergens ◽  
Adjuvant Effect ◽  
Recurrent Wheezing

Abstract Background: Exposure to cigarette smoke is causing health problems, its components are known to possess carcinogenic, mutagenic, cytotoxic or irritant properties. Prevalence of smoking in pregnant women is between 17% and 35% worldwide. Passive smoking is identified as a factor with negative impact on health, and children are especially vulnerable. Children raised in families with smokers have a higher incidence of respiratory infections, recurrent wheezing, bronchitis, nocturnal cough and asthma. The aim of this study was determination of sensitization to various allergens in children exposed to cigarette smoke compared with children not exposed to cigarette smoke. Material and method: One-hundred eighty children treated in Pediatric Clinic 1 of Tîrgu Mureș were included in the study between 2008- 2011. The patients were divided into two groups: 50 children exposed to cigarette smoke and 130 children not exposed. Measurement of lung function was performed in children over 4 years using a spirometer. Serum specific IgE was analyzed to inhalatory and food allergens. Wheezing phenotype was determined in children younger than 4 years and exposure to cigarette smoke was evaluated based on parents' responses to questionnaires. Results: There was a significantly greater likelihood of developing sensitivity in children exposed to tobacco smoke than in those not exposed to dermatophagoides pteronissimus, dermatophagoides farinae, milk and grass pollen. Conclusions: During early childhood both pre- and postnatal tobacco smoke exposure has an adjuvant effect on allergic sensitization inhalatory and food allergens.

Cigarette Smoke Exposure and Acute Respiratory Infection in Children Under Five: A Meta-Analysis

2020 ◽  
Author(s):  
Maya Ayu Riestiyowati ◽  
◽  
Setyo Sri Rahardjo ◽  
Vitri Widyaningsih ◽  
◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Respiratory Infection ◽  
Tobacco Smoke ◽  
Acute Respiratory Infection ◽  
Meta Analysis ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Children Under Five ◽  
Under Five

Background: Acute Respiratory Infections are classified into the upper and lower respiratory tract infections, contributing to the leading cause of death among children under five globally. The estimation showed the deaths of more than 800,000 children under five every year or about 2,200 per day. One of the risk factors for ARI in children under five years of age is secondary exposure to tobacco smoke. This study aimed to examine the effect of cigarette smoke exposure and acute respiratory infection in children under five. Subjects and Method: This was meta analysis and systematic review. The study was conducted by collecting published articles from Google Scholar, Pubmed, and Springer Link databases, from year 2010 to 2019. Keywords used “risk factor” OR “passive smoking” OR “secondhand smoking” AND “ARI due to children under five”. The inclusion criteria were full text, using English language, using cross-sectional study design, and reporting adjusted odds ratio. The collected articles were selected by PRISMA flow chart. The quantitative data were analyzed by fixed effect model using Revman 5.3. Results: 6 studies from Cameroon, Ethiopia, India, Nepal, and Nigeria reported that tobacco smoke exposure increased the risk of acute respiratory infection in children under five (aOR=1.39; 95% CI= 1.22 to 1.58; p<0.001). Conclusion: Tobacco smoke exposure increases the risk of acute respiratory infection in children under five. Keywords: tobacco smoke, acute respiratory infection, children under five Correspondence: Maya Ayu Riestiyowati. Masters Program in Public Health. Universitas Sebelas Maret, Jl. Ir. Sutami 36A, Surakarta 57126, Central Java. Email: [email protected]. Mobile: 081235840067.

scholarly journals Tobacco smoke exposure and endothelial dysfunction in patients with advanced coronary artery disease

2013 ◽  
Vol 123 (9) ◽  
pp. 474-481 ◽  
Author(s):  
Dorota Szpak ◽  
Andrzej Grochowalski ◽  
Ryszard Chrząszcz ◽  
Ewa Florek ◽  
Wojciech Jawień ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Endothelial Dysfunction ◽  
Tobacco Smoke ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Artery Disease ◽  
Advanced Coronary Artery Disease

Cigarette smoke exposure potentiates bleomycin-induced lung fibrosis in guinea pigs

2003 ◽  
Vol 285 (4) ◽  
pp. L949-L956 ◽  
Author(s):  
José Cisneros-Lira ◽  
Miguel Gaxiola ◽  
Carlos Ramos ◽  
Moisés Selman ◽  
Annie Pardo
Keyword(s):  
Cigarette Smoke ◽  
Tobacco Smoke ◽  
Guinea Pigs ◽  
Lung Fibrosis ◽  
Smooth Muscle Actin ◽  
Smoke Exposure ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Tobacco Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Fibroblast Proliferation

The role of tobacco smoking in the development and outcome of pulmonary fibrosis is uncertain. To approach the effects of cigarette smoke on bleomycin-induced lung fibrosis, we studied five groups of guinea pigs: 1) controls, 2) instilled with bleomycin (B), 3) exposed to tobacco smoke for 6 wk (TS), 4) bleomycin instillation plus tobacco smoke exposure for 6 wk (B+TS), and 5) tobacco smoke exposure for 6 wk and bleomycin after smoking (TS/B). Guinea pigs receiving bleomycin and tobacco smoke exposure exhibited higher fibrotic lesions including a significant increase in the number of positive α-smooth muscle actin cells compared with bleomycin alone (B+TS, 3.4 ± 1.2%; TS/B, 3.7 ± 1.5%; B, 2.3 ± 1.5%; P < 0.01). However, only the TS/B group reached a significant increase in lung collagen compared with the bleomycin group (TS/B, 3.5 ± 0.7; B ± TS, 2.9 ± 0.4; B, 2.4 ± 0.2 mg hydroxyproline/lung; P < 0.01). Bronchoalveolar lavage (BAL) from TS/B showed an increased number of eosinophils and higher levels of IL-4 and tissue inhibitor of metalloproteinase-2 ( P < 0.01 for all comparisons) and induced a significant increase in fibroblast proliferation ( P < 0.05). Importantly, smoke exposure alone induced an increase in BAL neutrophils, matrix metalloproteinase-9, and fibroblast proliferation compared with controls, suggesting that tobacco smoke creates a profibrotic milieu that may contribute to the increased bleomycin-induced fibrosis.

scholarly journals An Analysis of the Role of Tobacco-Specific Nitrosamines in the Carcinogenicity of Tobacco Smoke

2003 ◽  
Vol 1 (2) ◽  
pp. 154014203914343 ◽  
Author(s):  
Buddy G. Brown ◽  
August J. Borschke ◽  
David J. Doolittle
Keyword(s):  
Cigarette Smoke ◽  
Dna Adducts ◽  
Tobacco Smoke ◽  
Complex Mixture ◽  
Tobacco Smoke Exposure ◽  
In Vivo Studies ◽  
Laboratory Animals ◽  
Causative Role ◽  
Mainstream Smoke ◽  
Tobacco Specific Nitrosamines

Cigarette smoke is a complex mixture consisting of more than 4500 chemicals, including several tobacco-specific nitrosamines (TSNA). TSNA typically form in tobacco during the post-harvest period, with some fraction being transferred into mainstream smoke when a cigarette is burned during use. The most studied of the TSNA is 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). NNK has been shown to be carcinogenic in laboratory animals. Studies examining the carcinogenicity of NNK frequently are conducted by injecting rodents with a single dose of 2.5 to 10 μmol of pure NNK; the amount of NNK contained in all of the mainstream smoke from about 3700 to 14,800 typical U.S. cigarettes. Extrapolated to a 70-kg smoker, the carcinogenic dose of pure NNK administered to rodents would be equivalent to the amount of NNK in all of the mainstream smoke of 22 to 87 million typical U.S. cigarettes. Furthermore, extrapolating results from rodent studies based on a single injection of pure NNK to establish a causative role for NNK in the carcinogenicity of chronic tobacco smoke exposure in humans is not consistent with basic pharmacological and toxicological principles. For example, such an approach fails to consider the effect of other smoke constituents upon the toxicity of NNK. In vitro studies demonstrate that nicotine, cotinine, and aqueous cigarette “tar” extract (ACTE) all inhibit the mutagenic activity of NNK. In vivo studies reveal that the formation of pulmonary DNA adducts in mice injected with NNK is inhibited by the administration of cotinine and mainstream cigarette smoke. Cigarette smoke has been shown to modulate the metabolism of NNK, providing a mechanism for the inhibitory effects of cigarette smoke and cigarette smoke constituents on NNK-induced tumorigenesis. NNK-related pulmonary DNA adducts have not been detected in rodents exposed to cigarette smoke, nor has the toxicity of tobacco smoke or tobacco smoke condensate containing marked reductions in TSNA concentrations been shown to be reduced in any biological assay. In summary, there is no experimental evidence to suggest that reduction of TSNA will reduce the mutagenic, cytotoxic, or carcinogenic potential of tobacco smoke.

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