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...

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Main Authors: Kumboyono Kumboyono, Indah N. Chomsy, Nadya N. Shalshabilla, Hidayat Sujuti, Arie Srihardyastutie, Cholid T. Tjahjono, Teuku Heriansyah, Titin A. Wihastuti
Format: Article
Language:English
Published: European Publishing 2024-01-01
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.
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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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