Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysis
Introduction The main alkaloid component in cigarettes is nicotine. Cotinine, a metabolite of nicotine, is capable of causing dependence effects through endless mechanisms modulated by the ion channel nicotinic acetylcholine receptors nAChRs. Nicotine and cotinine can also cause damage to blood vess...
Main Authors: | , , , , , , , |
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Format: | Article |
Language: | English |
Published: |
European Publishing
2024-01-01
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Series: | Tobacco Induced Diseases |
Subjects: | |
Online Access: | https://www.tobaccoinduceddiseases.org/Nicotine-is-associated-with-smoking-dependence-and-vascular-ninflammation-through,171356,0,2.html |
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author | Kumboyono Kumboyono Indah N. Chomsy Nadya N. Shalshabilla Hidayat Sujuti Arie Srihardyastutie Cholid T. Tjahjono Teuku Heriansyah Titin A. Wihastuti |
author_facet | Kumboyono Kumboyono Indah N. Chomsy Nadya N. Shalshabilla Hidayat Sujuti Arie Srihardyastutie Cholid T. Tjahjono Teuku Heriansyah Titin A. Wihastuti |
author_sort | Kumboyono Kumboyono |
collection | DOAJ |
description | Introduction
The main alkaloid component in cigarettes is nicotine. Cotinine, a
metabolite of nicotine, is capable of causing dependence effects through endless
mechanisms modulated by the ion channel nicotinic acetylcholine receptors
nAChRs. Nicotine and cotinine can also cause damage to blood vessels through
a chronic inflammatory process mediated by the Ligand-Tie2 Angiopoietin
Receptor system. Hypoxic conditions that occur due to vascular inflammation
cause a decrease in the concentration of nitric oxide (NO). This study aimed to
evaluate the relationship between NO levels and cotinine through the expression
of nAChRs that mediate the nicotine dependence mechanism and Tie2 (Tyrosine
Kinase 2) expression.
Methods
A cross-sectional study was conducted with 200 participants grouped into
two groups based on their smoking status: 100 smokers and 100 non-smokers.
All participants were men aged 20–40 years with no history of cardiovascular
disease, diabetes mellitus, or dyslipidemia, and were not currently on medication.
According to the parameters used, all blood samples were taken from peripheral
blood for analysis using the ELISA kit or Colorimetric Assay Kit.
Results
Cigarette consumption increases blood cotinine concentrations in smokers
and causes dependence by modulating nAChRs. The study indicates an emerging
cycle regarding nicotine–cotinine consumption and nAChRs expression. In
addition, the data in this study showed a significant relationship (p<0.001)
regarding the cycle formed with decreased NO levels as a result of damage caused
by Tie2-mediated inflammation.
Conclusions
There is a relationship between NO levels and cotinine through
nAChRs, which mediate the nicotine dependence mechanism and Tie2 expression. |
first_indexed | 2024-03-08T03:06:09Z |
format | Article |
id | doaj.art-9d0c018801454a63b273dc3521dbf6f6 |
institution | Directory Open Access Journal |
issn | 1617-9625 |
language | English |
last_indexed | 2024-03-08T03:06:09Z |
publishDate | 2024-01-01 |
publisher | European Publishing |
record_format | Article |
series | Tobacco Induced Diseases |
spelling | doaj.art-9d0c018801454a63b273dc3521dbf6f62024-02-13T09:09:30ZengEuropean PublishingTobacco Induced Diseases1617-96252024-01-0122January1910.18332/tid/171356171356Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysisKumboyono Kumboyono0https://orcid.org/0000-0003-2124-8673Indah N. Chomsy1https://orcid.org/0000-0002-1050-3571Nadya N. Shalshabilla2https://orcid.org/0009-0005-8248-6167Hidayat Sujuti3https://orcid.org/0000-0001-8155-0036Arie Srihardyastutie4https://orcid.org/0000-0002-8462-4632Cholid T. Tjahjono5https://orcid.org/0000-0002-6766-2792Teuku Heriansyah6https://orcid.org/0000-0002-0363-1997Titin A. Wihastuti7https://orcid.org/0000-0002-1419-7225Department of Nursing, Faculty of Health Sciences, University of Brawijaya, Malang, IndonesiaDoctoral Program of Medical Science, Faculty of Medicine, University of Brawijaya, Malang, IndonesiaMaster Program of Biomedical Science, Faculty of Medicine, University of Brawijaya, Malang, IndonesiaDepartment of Biomolecular-Ophtalmology, Faculty of Medicine, University of Brawijaya-Saiful Anwar General Hospital, Malang, IndonesiaDepartment of Chemistry, Faculty of Mathematics and Natural Science, University of Brawijaya, Malang, IndonesiaDepartment of Cardiology and Vascular Medicine, Faculty of Medicine, University of Brawijaya-Saiful Anwar General Hospital, Malang, IndonesiaDepartment of Cardiology and Vascular Medicine, Syiah Kuala University, Banda Aceh, IndonesiaDepartment of Nursing, Faculty of Health Sciences, University of Brawijaya, Malang, IndonesiaIntroduction The main alkaloid component in cigarettes is nicotine. Cotinine, a metabolite of nicotine, is capable of causing dependence effects through endless mechanisms modulated by the ion channel nicotinic acetylcholine receptors nAChRs. Nicotine and cotinine can also cause damage to blood vessels through a chronic inflammatory process mediated by the Ligand-Tie2 Angiopoietin Receptor system. Hypoxic conditions that occur due to vascular inflammation cause a decrease in the concentration of nitric oxide (NO). This study aimed to evaluate the relationship between NO levels and cotinine through the expression of nAChRs that mediate the nicotine dependence mechanism and Tie2 (Tyrosine Kinase 2) expression. Methods A cross-sectional study was conducted with 200 participants grouped into two groups based on their smoking status: 100 smokers and 100 non-smokers. All participants were men aged 20–40 years with no history of cardiovascular disease, diabetes mellitus, or dyslipidemia, and were not currently on medication. According to the parameters used, all blood samples were taken from peripheral blood for analysis using the ELISA kit or Colorimetric Assay Kit. Results Cigarette consumption increases blood cotinine concentrations in smokers and causes dependence by modulating nAChRs. The study indicates an emerging cycle regarding nicotine–cotinine consumption and nAChRs expression. In addition, the data in this study showed a significant relationship (p<0.001) regarding the cycle formed with decreased NO levels as a result of damage caused by Tie2-mediated inflammation. Conclusions There is a relationship between NO levels and cotinine through nAChRs, which mediate the nicotine dependence mechanism and Tie2 expression.https://www.tobaccoinduceddiseases.org/Nicotine-is-associated-with-smoking-dependence-and-vascular-ninflammation-through,171356,0,2.htmlnicotinecotininevascular inflammationoxidative stresstobacco-induced disease |
spellingShingle | Kumboyono Kumboyono Indah N. Chomsy Nadya N. Shalshabilla Hidayat Sujuti Arie Srihardyastutie Cholid T. Tjahjono Teuku Heriansyah Titin A. Wihastuti Nicotine is associated with smoking dependence and vascular inflammation through cotinine: A mediation analysis Tobacco Induced Diseases nicotine cotinine vascular inflammation oxidative stress tobacco-induced disease |
title | Nicotine is associated with smoking dependence and vascular
inflammation through cotinine: A mediation analysis |
title_full | Nicotine is associated with smoking dependence and vascular
inflammation through cotinine: A mediation analysis |
title_fullStr | Nicotine is associated with smoking dependence and vascular
inflammation through cotinine: A mediation analysis |
title_full_unstemmed | Nicotine is associated with smoking dependence and vascular
inflammation through cotinine: A mediation analysis |
title_short | Nicotine is associated with smoking dependence and vascular
inflammation through cotinine: A mediation analysis |
title_sort | nicotine is associated with smoking dependence and vascular inflammation through cotinine a mediation analysis |
topic | nicotine cotinine vascular inflammation oxidative stress tobacco-induced disease |
url | https://www.tobaccoinduceddiseases.org/Nicotine-is-associated-with-smoking-dependence-and-vascular-ninflammation-through,171356,0,2.html |
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