Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Cigarette Smoke-Induced Oxidative Stress and Its Related Molecular/Cellular Events
share announcement

Cigarette Smoke-Induced Oxidative Stress and Its Related Molecular/Cellular Events

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 (31 May 2023) | Viewed by 8577

Special Issue Editor

Prof. Dr. Moo-Yeol Lee

E-Mail Website
Guest Editor
College of Pharmacy, Dongguk University, Seoul, Republic of Korea
Interests: smoking; cigarette smoke; redox signal; oxidative stress; toxicity; cardiovascular diseases

Special Issue Information

Dear Colleagues,

Smoking is a well-established risk factor for respiratory disorders, cardiovascular diseases, and cancers. In the past few decades, many studies have revealed smoking-induced toxicological events. Although a number of events are involved in the pathogenic processes, the molecular bases of these events have yet to be fully elucidated. Among diverse toxicological events, oxidative stress is one of the most widely recognized factors contributing to this pathogenesis.

Cigarette smoke contains free radicals and prooxidants. It also generates reactive oxygen species through the chemical reactions with biomolecules. In addition, it is capable of stimulating cells or tissues to produce reactive oxygen species. Therefore, cigarette smoke causes the oxidative modification of macromolecules such as protein, lipid, and DNA, and thus disturbs their functions. It thereby damages antioxidant systems, upsets the redox balance, and induces the dysregulation of redox signaling, ultimately leading to cytotoxicity. However, numerous issues still need further clarification, including the molecular mechanisms underlying reactive oxygen species generation or oxidative stress, the mechanistic links between oxidative stress and toxicological consequences, and the constituents in cigarette smoke responsible for oxidative stress.

This Special Issue is open to a wide range of subjects exploring cigarette-smoke-induced oxidative stress and its related molecular/cellular events, with emphasis on mechanistic insights. There are no limitations on the types of study and manuscript: in vitro, in vivo, translational, or clinical studies and research article, review, or any other types of manuscript, provided they pertain to relevant topics with scientific merit. It is highly encouraged to submit studies on heated tobacco products and electronic cigarettes in addition to conventional cigarettes.

I look forward to receiving your contributions.

Prof. Dr. Moo-Yeol Lee
Guest Editor

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

  • smoking
  • cigarette smoke
  • oxidative stress
  • reactive oxygen species
  • redox signal
  • toxicity
  • mechanism

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

19 pages, 2758 KiB  
Article
Maqui Berry and Ginseng Extracts Reduce Cigarette Smoke-Induced Cell Injury in a 3D Bone Co-Culture Model
by Huizhi Guo, Weidong Weng, Shuncong Zhang, Helen Rinderknecht, Bianca Braun, Regina Breinbauer, Purva Gupta, Ashok Kumar, Sabrina Ehnert, Tina Histing, Andreas K. Nussler and Romina H. Aspera-Werz
Antioxidants 2022, 11(12), 2460; https://doi.org/10.3390/antiox11122460 - 14 Dec 2022
Cited by 9 | Viewed by 1787
Abstract
Cigarette smoking-induced oxidative stress has harmful effects on bone metabolism. Maqui berry extract (MBE) and ginseng extract (GE) are two naturally occurring antioxidants that have been shown to reduce oxidative stress. By using an osteoblast and osteoclast three-dimensional co-culture system, we investigated the [...] Read more.
Cigarette smoking-induced oxidative stress has harmful effects on bone metabolism. Maqui berry extract (MBE) and ginseng extract (GE) are two naturally occurring antioxidants that have been shown to reduce oxidative stress. By using an osteoblast and osteoclast three-dimensional co-culture system, we investigated the effects of MBE and GE on bone cells exposed to cigarette smoke extract (CSE). The cell viability and function of the co-culture system were measured on day 14. Markers of bone cell differentiation and oxidative stress were evaluated at gene and protein levels on day 7. The results showed that exposure to CSE induced osteoporotic-like alterations in the co-culture system, while 1.5 µg/mL MBE and 50 µg/mL GE improved CSE-impaired osteoblast function and decreased CSE-induced osteoclast function. The molecular mechanism of MBE and GE in preventing CSE-induced bone cell damage is linked with the inhibition of the NF-κB signaling pathway and the activation of the Nrf2 signaling pathway. Therefore, MBE and GE can reduce CSE-induced detrimental effects on bone cells and, thus, prevent smoking-induced alterations in bone cell homeostasis. These two antioxidants are thus suitable supplements to support bone regeneration in smokers. Full article
(This article belongs to the Special Issue Cigarette Smoke-Induced Oxidative Stress and Its Related Molecular/Cellular Events)
►▼ Show Figures

Figure 1

Review

Jump to: Research

24 pages, 814 KiB  
Review
Cigarette Smoke-Induced Reactive Oxygen Species Formation: A Concise Review
by Yoon-Seok Seo, Jung-Min Park, Jae-Hyeong Kim and Moo-Yeol Lee
Antioxidants 2023, 12(9), 1732; https://doi.org/10.3390/antiox12091732 - 7 Sep 2023
Cited by 8 | Viewed by 1836
Abstract
Smoking is recognized as a significant risk factor for numerous disorders, including cardiovascular diseases, respiratory conditions, and various forms of cancer. While the exact pathogenic mechanisms continue to be explored, the induction of oxidative stress via the production of excess reactive oxygen species [...] Read more.
Smoking is recognized as a significant risk factor for numerous disorders, including cardiovascular diseases, respiratory conditions, and various forms of cancer. While the exact pathogenic mechanisms continue to be explored, the induction of oxidative stress via the production of excess reactive oxygen species (ROS) is widely accepted as a primary molecular event that predisposes individuals to these smoking-related ailments. This review focused on how cigarette smoke (CS) promotes ROS formation rather than the pathophysiological repercussions of ROS and oxidative stress. A comprehensive analysis of existing studies revealed the following key ways through which CS imposes ROS burden on biological systems: (1) ROS, as well as radicals, are intrinsically present in CS, (2) CS constituents generate ROS through chemical reactions with biomolecules, (3) CS stimulates cellular ROS sources to enhance production, and (4) CS disrupts the antioxidant system, aggravating the ROS generation and its functions. While the evidence supporting these mechanisms is chiefly based on in vitro and animal studies, the direct clinical relevance remains to be fully elucidated. Nevertheless, this understanding is fundamental for deciphering molecular events leading to oxidative stress and for developing intervention strategies to counter CS-induced oxidative stress. Full article
(This article belongs to the Special Issue Cigarette Smoke-Induced Oxidative Stress and Its Related Molecular/Cellular Events)
►▼ Show Figures

Figure 1

30 pages, 932 KiB  
Review
Cigarette Smoke-Induced Respiratory Response: Insights into Cellular Processes and Biomarkers
by Sang-Ryul Cha, Jimin Jang, Sung-Min Park, Se Min Ryu, Seong-Joon Cho and Se-Ran Yang
Antioxidants 2023, 12(6), 1210; https://doi.org/10.3390/antiox12061210 - 3 Jun 2023
Cited by 6 | Viewed by 4339
Abstract
Cigarette smoke (CS) poses a significant risk factor for respiratory, vascular, and organ diseases owing to its high content of harmful chemicals and reactive oxygen species (ROS). These substances are known to induce oxidative stress, inflammation, apoptosis, and senescence due to their exposure [...] Read more.
Cigarette smoke (CS) poses a significant risk factor for respiratory, vascular, and organ diseases owing to its high content of harmful chemicals and reactive oxygen species (ROS). These substances are known to induce oxidative stress, inflammation, apoptosis, and senescence due to their exposure to environmental pollutants and the presence of oxidative enzymes. The lung is particularly susceptible to oxidative stress. Persistent oxidative stress caused by chronic exposure to CS can lead to respiratory diseases such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis (PF), and lung cancer. Avoiding exposure to environmental pollutants, like cigarette smoke and air pollution, can help mitigate oxidative stress. A comprehensive understanding of oxidative stress and its impact on the lungs requires future research. This includes identifying strategies for preventing and treating lung diseases as well as investigating the underlying mechanisms behind oxidative stress. Thus, this review aims to investigate the cellular processes induced by CS, specifically inflammation, apoptosis, senescence, and their associated biomarkers. Furthermore, this review will delve into the alveolar response provoked by CS, emphasizing the roles of potential therapeutic target markers and strategies in inflammation and oxidative stress. Full article
(This article belongs to the Special Issue Cigarette Smoke-Induced Oxidative Stress and Its Related Molecular/Cellular Events)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop