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Cigarette Smoking: Associated Oxidative Stress and Health Hazards

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A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 April 2023) | Viewed by 24714

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Special Issue Editors

Prof. Dr. Philip M. Hansbro

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Guest Editor

1. School of Life Sciences, Univerity of Technology Sydney, NSW 2007, Australia
2. Centre for Inflammation, Centenary Institute, Sydney, NSW 2050, Australia
Interests: chronic respiratory diseases; animal models; lung microbiome; inflammasomes; miRNA

Dr. Keshav Raj Paudel

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Guest Editor

1. School of Life Sciences, Univerity of Technology Sydney, NSW 2007, Australia
2. Centre for Inflammation, Centenary Institute, Sydney, NSW 2050, Australia
Interests: chronic respiratory diseases; in vitro assays; cellular and molecular biology; pharmacology; animal models; lung cancer
Special Issues, Collections and Topics in MDPI journals

Dr. Vivek Dharwal

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Guest Editor

1. School of Life Sciences, Univerity of Technology Sydney, NSW 2007, Australia
2. Centre for Inflammation, Centenary Institute, Sydney, NSW 2050, Australia
Interests: chronic respiratory diseases; oxidative stress; mitochondrial dysfunction; pharmacology; pre-clinical animal models

Special Issue Information

Dear Colleagues,

Tobacco use is one of the most significant public health hazards facing today's world. According to a report by the World Health Organization, tobacco kills half of its users. Approximately 8 million tobacco users (7 million direct users and 1.2 million exposed to second-hand smoke) die each year owing to different health complications. Among the types of tobacco use, cigarette smoking is the most common. Typically, cigarette smoke (CS) contains thousands of harmful chemicals, such as reactive oxygen species (ROS), tar, and particulate matter, which result in the orchestration of disease-related symptoms. Tobacco smoking is the primary risk factor for the development of chronic inflammatory lung diseases (asthma, chronic obstructive pulmonary disease). Chronic exposure to cigarette smoke activates different cellular pathways that result in inflammation, cellular metabolic shifts, oxidative stress, protease–antiprotease, and cellular apoptosis in the lungs. In addition to chronic lung diseases, cigarette smoking leads to the development of cardiovascular diseases. According to the literature, cigarette smoking doubles the risk of developing acute myocardial infarction, cerebrovascular disease, and heart failure. Further, the association of cigarette smoking with the development of chronic kidney diseases is now known. Accordingly, research is ongoing to better understand the molecular impact of cigarette smoke exposure and to develop new therapeutics.

This Special Issue aims to cover the recent in vitro, in vivo, and clinical research updates in the field of cigarette-smoke-induced health disorders. Original articles, short communications, and reviews related to these topics are welcome for submission.

Prof. Dr. Philip M. Hansbro
Dr. Keshav Raj Paudel
Dr. Vivek Dharwal
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

chronic respiratory diseases
cigarette smoking
animal model
in vitro
clinical study
oxidative stress
antioxidants

Published Papers (7 papers)

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Research

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11 pages, 2739 KiB

Open AccessCommunication

Relationships between Serum Biomarkers of Oxidative Stress and Tobacco Smoke Exposure in Patients with Mental Disorders

by Ana-Maria Vlasceanu, Daniela Gradinaru, Miriana Stan, Viorela G. Nitescu and Daniela Luiza Baconi

Antioxidants 2023, 12(6), 1299; https://doi.org/10.3390/antiox12061299 - 19 Jun 2023

Viewed by 2630

Abstract

The role of cigarette smoking as an aggravating factor of systemic oxidative stress in patients with mental disorders has not been extensively investigated, although significantly higher rates of smoking are recorded in these subjects in comparison with the general population. In the present study, we tested the hypothesis that smoking might be an exacerbator of systemic oxidative stress, being directly correlated with the degree of exposure to tobacco smoke. We analyzed, in 76 adult subjects from a public health care unit, the relationships between serum cotinine levels as a marker of tobacco smoke exposure, and three biomarkers of oxidative stress: the serum glutathione (GSH), the advanced oxidation protein products (AOPPs), and the total serum antioxidant status (FRAP). The results indicate that the degree of tobacco smoke exposure was inversely associated with GSH levels in both passive and active smokers, suggesting that smoke particulate components’ toxicity is associated with a systemic GSH depletion. Paradoxically, the lowest AOPP levels which were positively associated with GSH, were recorded in active smoking patients whereas in passive smokers individual values of AOPPs decreased along with the increase in GSH levels. Our data suggest that an enhanced inhalation of particulate constituents of cigarette smoke could induce critical changes in systemic redox homeostasis and GSH can no longer exert its antioxidant role. Full article

(This article belongs to the Special Issue Cigarette Smoking: Associated Oxidative Stress and Health Hazards)

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15 pages, 2983 KiB

Open AccessArticle

Red- and Near-Infrared-Excited Autofluorescence as a Marker for Acute Oxidative Stress in Skin Exposed to Cigarette Smoke Ex Vivo and In Vivo

by Phuong Thao Tran, Parichat Tawornchat, Burkhard Kleuser, Silke B. Lohan, Johannes Schleusener, Martina C. Meinke and Maxim E. Darvin

Antioxidants 2023, 12(5), 1011; https://doi.org/10.3390/antiox12051011 - 27 Apr 2023

Cited by 2 | Viewed by 1673

Abstract

Air pollution is increasing worldwide and skin is exposed to high levels of pollution daily, causing oxidative stress and other negative consequences. The methods used to determine oxidative stress in the skin are invasive and non-invasive label-free in vivo methods, which are severely limited. Here, a non-invasive and label-free method to determine the effect of cigarette smoke (CS) exposure on skin ex vivo (porcine) and in vivo (human) was established. The method is based on the measurement of significant CS-exposure-induced enhancement in red- and near-infrared (NIR)-excited autofluorescence (AF) intensities in the skin. To understand the origin of red- and NIR-excited skin AF, the skin was exposed to several doses of CS in a smoking chamber. UVA irradiation was used as a positive control of oxidative stress in the skin. The skin was measured with confocal Raman microspectroscopy before CS exposure, immediately after CS exposure, and after skin cleaning. CS exposure significantly increased the intensity of red- and NIR-excited skin AF in a dose-dependent manner in the epidermis, as confirmed by laser scanning microscopy AF imaging and fluorescence spectroscopy measurements. UVA irradiation enhanced the intensity of AF, but to a lower extent than CS exposure. We concluded that the increase in red- and NIR-excited AF intensities of the skin after CS exposure could clearly be related to the induction of oxidative stress in skin, where skin surface lipids are mainly oxidized. Full article

(This article belongs to the Special Issue Cigarette Smoking: Associated Oxidative Stress and Health Hazards)

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18 pages, 2569 KiB

Open AccessArticle

Camellia sinensis L. Alleviates Pulmonary Inflammation Induced by Porcine Pancreas Elastase and Cigarette Smoke Extract

by Dong-Uk Shin, Ji-Eun Eom, Hyeon-Ji Song, Sun Young Jung, Thi Van Nguyen, Kyung Min Lim, Ok Hee Chai, Hyun-Jin Kim, Gun-Dong Kim, Hee Soon Shin and So-Young Lee

Antioxidants 2022, 11(9), 1683; https://doi.org/10.3390/antiox11091683 - 28 Aug 2022

Cited by 6 | Viewed by 2542

Abstract

Cigarette smoke (CS) is the major factor in the development of chronic obstructive pulmonary disease (COPD), the third leading cause of death worldwide. Furthermore, although Camellia sinensis (CN) has been known as an anti-inflammatory material, the effect of CN has not yet been known on pulmonary inflammation in COPD. Thus, we investigated the protective effects of Camellia sinensis L. extract (CLE) against pulmonary inflammation in porcine pancreas elastase (PPE) and a cigarette smoke extract (CSE)-induced COPD mouse model. Oral administration of CLE suppressed the symptoms such as infiltration of immune cells, cytokines/chemokines secretion, mucus hypersecretion, and injuries of the lung parenchyma. Increased inflammatory responses in COPD are mediated by various immune cells such as airway epithelial cells, neutrophils, and alveolar macrophages. Thus, we investigated the effect and mechanisms of CLE in H292, HL-60, and MH-S cells. The CLE inhibited the expression of IL-6, IL-8, MUC5AC and MUC5B on CSE/LPS-stimulated H292 cells and also suppressed the formation of neutrophil extracellular traps and secretion of neutrophil elastase by inhibiting reactive oxygen species in PMA-induced HL-60 cells. In particular, the CLE suppressed the release of cytokines and chemokines caused by activating the nuclear factor kappa-light-chain-enhancer of activated B via the activation of nuclear factor erythroid-2-related factor 2 and the heme oxygenase-1 pathway in CSE/LPS-stimulated MH-S cells. Therefore, we suggest that the CLE administration be the effective approach for treating or preventing chronic pulmonary diseases such as COPD induced by CS. Full article

(This article belongs to the Special Issue Cigarette Smoking: Associated Oxidative Stress and Health Hazards)

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12 pages, 1471 KiB

Open AccessArticle

by Leonardo Schirone, Lorenzo Loffredo, Roberto Carnevale, Simona Battaglia, Roberta Marti, Stefano Pizzolo, Simona Bartimoccia, Cristina Nocella, Vittoria Cammisotto, Wael Saade, Alessandra Tanzilli, Sebastiano Sciarretta, Isotta Chimenti, Elena De Falco, Elena Cavarretta, Vittorio Picchio, Mariangela Peruzzi, Antonino Marullo, Fabio Miraldi, Francesco Violi, Andrea Morelli, Giuseppe Biondi-Zoccai and Giacomo Frati Show full author list Hide full author list

Antioxidants 2022, 11(7), 1237; https://doi.org/10.3390/antiox11071237 - 24 Jun 2022

Cited by 1 | Viewed by 2044

Abstract

Smoking is still a major cardiovascular risk factor, despite many public awareness campaigns and dedicated interventions. Recently, modified risk products (MRP), e.g., heat-not-burn cigarettes (HNBCs), have been introduced as surrogates of traditional combustion cigarettes (TCCs). Although these products are promoted as healthier than TCCs, few studies have been conducted to assess it. This work is a sex-focused sub-study of a prospective observational study in which apparently healthy chronic TCC smokers were age-matched with regular HNBC users. Blood samples were collected for biochemical assays and blood pressure and flow-mediated dilation (FMD) were measured. Out of 60 subjects, 33 (55%) were women, and 27 (45%) men, with 11 (33%) vs. 9 (33%) non-smokers, respectively, 10 (30%) vs. 10 (37%) TCC smokers, and 12 (36%) vs. 8 (30%) HNBC smokers (p = 0.946). Bivariate and multivariable analyses showed no statistically significant between-sex differences in NO, H₂O₂, sCD40L, sNox2-dp, sP-selectin, platelet aggregation, cotinine or FMD, overall, in non-smokers, in TCC smokers, or in HNBC smokers (all p > 0.05). HNBCs appeared safer than TCCs when focusing on Nox2-dp (p = 0.026) and sP-selectin (p = 0.050) but had similar levels of the other measured markers. In conclusion, HNBCs have similar detrimental effects on women and men’s oxidative stress (H₂O₂: p = 0.49; sNox2-dp: p = 0.31) and platelet activation (sP-selectin: p = 0.33; platelet aggregation p = 0.87). Full article

(This article belongs to the Special Issue Cigarette Smoking: Associated Oxidative Stress and Health Hazards)

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18 pages, 4181 KiB

Open AccessArticle

Attenuation of Cigarette-Smoke-Induced Oxidative Stress, Senescence, and Inflammation by Berberine-Loaded Liquid Crystalline Nanoparticles: In Vitro Study in 16HBE and RAW264.7 Cells

by Keshav Raj Paudel, Nisha Panth, Bikash Manandhar, Sachin Kumar Singh, Gaurav Gupta, Peter R. Wich, Srinivas Nammi, Ronan MacLoughlin, Jon Adams, Majid Ebrahimi Warkiani, Dinesh Kumar Chellappan, Brian G. Oliver, Philip M. Hansbro and Kamal Dua

Antioxidants 2022, 11(5), 873; https://doi.org/10.3390/antiox11050873 - 28 Apr 2022

Cited by 27 | Viewed by 5684

Abstract

Cigarette smoke is considered a primary risk factor for chronic obstructive pulmonary disease. Numerous toxicants present in cigarette smoke are known to induce oxidative stress and airway inflammation that further exacerbate disease progression. Generally, the broncho-epithelial cells and alveolar macrophages exposed to cigarette smoke release massive amounts of oxidative stress and inflammation mediators. Chronic exposure of cigarette smoke leads to premature senescence of airway epithelial cells. This impairs cellular function and ultimately leads to the progression of chronic lung diseases. Therefore, an ideal therapeutic candidate should prevent disease progression by controlling oxidative stress, inflammation, and senescence during the initial stage of damage. In our study, we explored if berberine (an alkaloid)-loaded liquid crystalline nanoparticles (berberine-LCNs)-based treatment to human broncho-epithelial cells and macrophage inhibits oxidative stress, inflammation, and senescence induced by cigarette-smoke extract. The developed berberine-LCNs were found to have favourable physiochemical parameters, such as high entrapment efficiency and sustained in vitro release. The cellular-assay observations revealed that berberine-LCNs showed potent antioxidant activity by suppressing the generation of reactive oxygen species in both broncho-epithelial cells (16HBE) and macrophages (RAW264.7), and modulating the genes involved in inflammation and oxidative stress. Similarly, in 16HBE cells, berberine-LCNs inhibited the cigarette smoke-induced senescence as revealed by X-gal staining, gene expression of CDKN1A (p21), and immunofluorescent staining of p21. Further in-depth mechanistic investigations into antioxidative, anti-inflammatory, and antisenescence research will diversify the current findings of berberine as a promising therapeutic approach for inflammatory lung diseases caused by cigarette smoking. Full article

(This article belongs to the Special Issue Cigarette Smoking: Associated Oxidative Stress and Health Hazards)

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13 pages, 904 KiB

Open AccessArticle

Quercetin Improves Pulmonary Function and Prevents Emphysema Caused by Exposure to Cigarette Smoke in Male Mice

by Natália Pereira da Silva Araújo, Natália Alves de Matos, Michel Oliveira, Ana Beatriz Farias de Souza, Thalles de Freitas Castro, Pedro Alves Machado-Júnior, Débora Maria Soares de Souza, André Talvani, Sílvia Dantas Cangussú, Rodrigo Cunha Alvim de Menezes and Frank Silva Bezerra

Antioxidants 2022, 11(2), 181; https://doi.org/10.3390/antiox11020181 - 18 Jan 2022

Cited by 12 | Viewed by 3970

Abstract

Chronic obstructive pulmonary disease (COPD) is the major cause of morbidity and mortality worldwide, and cigarette smoke is a key factor in the development of COPD. Thus, the development of effective therapies to prevent the advancement of COPD has become increasingly essential. We hypothesized that quercetin protects lungs in mice exposed to long-term cigarette smoke. Thirty-five C57BL/6 mice were exposed to cigarette smoke (12 cigarettes per day) for 60 days and pretreated with 10 mg/kg/day of quercetin via orogastric gavage. After the experimental protocol, the animals were euthanized and samples were collected for histopathological, antioxidant defense, oxidative stress and inflammatory analysis. The animals exposed to cigarette smoke showed an increase in respiratory rate and hematological parameters, cell influx into the airways, oxidative damage and inflammatory mediators, besides presenting with alterations in the pulmonary histoarchitecture. The animals receiving 10 mg/kg/day of quercetin that were exposed to cigarette smoke presented a reduction in cellular influx, less oxidative damage, reduction in cytokine levels, improvement in the histological pattern and improvement in pulmonary emphysema compared to the group that was only exposed to cigarette smoke. These results suggest that quercetin may be an agent in preventing pulmonary emphysema induced by cigarette smoke. Full article

(This article belongs to the Special Issue Cigarette Smoking: Associated Oxidative Stress and Health Hazards)

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Review

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20 pages, 2113 KiB

Open AccessReview

Protective Effects of Diets Rich in Polyphenols in Cigarette Smoke (CS)-Induced Oxidative Damages and Associated Health Implications

by Mithun Rudrapal, Siddhartha Maji, Shiv Kumar Prajapati, Payal Kesharwani, Prashanta Kumar Deb, Johra Khan, Randa Mohamed Ismail, Rani S. Kankate, Ranjan Kumar Sahoo, Shubham J. Khairnar and Atul R. Bendale

Antioxidants 2022, 11(7), 1217; https://doi.org/10.3390/antiox11071217 - 21 Jun 2022

Cited by 12 | Viewed by 4131

Abstract

Cigarette smoking has been responsible for causing many life-threatening diseases such as pulmonary and cardiovascular diseases as well as lung cancer. One of the prominent health implications of cigarette smoking is the oxidative damage of cellular constituents, including proteins, lipids, and DNA. The oxidative damage is caused by reactive oxygen species (ROS, oxidants) present in the aqueous extract of cigarette smoke (CS). In recent years, there has been considerable interest in the potential health benefits of dietary polyphenols as natural antioxidant molecules. Epidemiological studies strongly suggest that long-term consumption of diets (fruits, vegetables, tea, and coffee) rich in polyphenols offer protective effects against the development of cancer, cardiovascular diseases, diabetes, osteoporosis, and neurodegenerative diseases. For instance, green tea has chemopreventive effects against CI-induced lung cancer. Tea might prevent CS-induced oxidative damages in diseases because tea polyphenols, such as catechin, EGCG, etc., have strong antioxidant properties. Moreover, apple polyphenols, including catechin and quercetin, provide protection against CS-induced acute lung injury such as chronic obstructive pulmonary disease (COPD). In CS-induced health problems, the antioxidant action is often accompanied by the anti-inflammatory effect of polyphenols. In this narrative review, the CS-induced oxidative damages and the associated health implications/pathological conditions (or diseases) and the role of diets rich in polyphenols and/or dietary polyphenolic compounds against various serious/chronic conditions of human health have been delineated. Full article

(This article belongs to the Special Issue Cigarette Smoking: Associated Oxidative Stress and Health Hazards)

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