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: | , , , , , , , |
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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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| Summary: | 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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| ISSN: | 1617-9625 |