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Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers

Background: Exposure to cigarette smoke has been associated with pulmonary and reproductive dysfunctions; inflammatory response, oxidative stress and oxidative DNA damage induced by polycyclic aromatic hydrocarbons (PAHs) present in cigarette smoke have been implicated in the pathogenesis of these d...

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Autores principales: Nsonwu-Anyanwu, Augusta Chinyere, Egom, Ofem Ukwetan, Eworo, Raymond Ekong, Nsonwu, Magnus Chinonye, Aniekpon, Uyime Fabian, Ekpo, Daniel Orok, Opara Usoro, Chinyere Adanna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Iran University of Medical Sciences 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9700422/
https://www.ncbi.nlm.nih.gov/pubmed/36447550
http://dx.doi.org/10.47176/mjiri.36.108
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author Nsonwu-Anyanwu, Augusta Chinyere
Egom, Ofem Ukwetan
Eworo, Raymond Ekong
Nsonwu, Magnus Chinonye
Aniekpon, Uyime Fabian
Ekpo, Daniel Orok
Opara Usoro, Chinyere Adanna
author_facet Nsonwu-Anyanwu, Augusta Chinyere
Egom, Ofem Ukwetan
Eworo, Raymond Ekong
Nsonwu, Magnus Chinonye
Aniekpon, Uyime Fabian
Ekpo, Daniel Orok
Opara Usoro, Chinyere Adanna
author_sort Nsonwu-Anyanwu, Augusta Chinyere
collection PubMed
description Background: Exposure to cigarette smoke has been associated with pulmonary and reproductive dysfunctions; inflammatory response, oxidative stress and oxidative DNA damage induced by polycyclic aromatic hydrocarbons (PAHs) present in cigarette smoke have been implicated in the pathogenesis of these disorders. The peak expiratory flow rate (PEFR), a biomarker of inflammation and oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG), tumor necrosis factor alpha (TNF-α)), reproductive hormones (testosterone (TST), luteinizing hormone (LH), follicle stimulating hormone (FSH)) cotinine and urinary PAH metabolite (1-hydroxypyrene (1-HOP)) were estimated in male active smokers. Methods: One hundred men aged 20-47 years, comprising 50 active male smokers and 50 non-smokers, were randomly recruited into this comparative cross-sectional study. The PEFR was measured using a peak flow meter, serum levels of cotinine, FSH, LH, TST, TNF-α, and urine 8-OHdG by enzyme-linked immunosorbent assay and 1-HOP by high-performance liquid chromatography. Data analysis was done using a t-test and correlation analysis at p≤0.05. Results: Smokers had significantly higher cotinine (49.73±31.76 versus 0.51±0.69 ng/ml, p≤0.001), 8-OHdG (16.34±12.10 versus 5.79±2.14 ng/ml, p≤0.001) and lower PEFR (309.20±56.05 versus 452.80±45.76 L/min, p≤0.001) and LH (5.75±2.06 versus 6.97±2.79 mIU/ml, p=0.015) compared to non-smokers. Duration of exposure to cigarette smoke correlated positively with cotinine (r=0.937, p≤0.001) and 1-HOP (r=0.813, p≤0.001) while cotinine correlated positively with 1-HOP (r=0.863, p≤0.001) only in smokers. Conclusion: Reduced lung function and luteinizing hormone and concurrent increase in oxidative DNA damage associated with exposure to cigarette smoke may suggest the involvement of PAH-induced DNA damage in the development of pulmonary and reproductive impairment in smokers.
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spelling pubmed-97004222022-11-28 Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers Nsonwu-Anyanwu, Augusta Chinyere Egom, Ofem Ukwetan Eworo, Raymond Ekong Nsonwu, Magnus Chinonye Aniekpon, Uyime Fabian Ekpo, Daniel Orok Opara Usoro, Chinyere Adanna Med J Islam Repub Iran Original Article Background: Exposure to cigarette smoke has been associated with pulmonary and reproductive dysfunctions; inflammatory response, oxidative stress and oxidative DNA damage induced by polycyclic aromatic hydrocarbons (PAHs) present in cigarette smoke have been implicated in the pathogenesis of these disorders. The peak expiratory flow rate (PEFR), a biomarker of inflammation and oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG), tumor necrosis factor alpha (TNF-α)), reproductive hormones (testosterone (TST), luteinizing hormone (LH), follicle stimulating hormone (FSH)) cotinine and urinary PAH metabolite (1-hydroxypyrene (1-HOP)) were estimated in male active smokers. Methods: One hundred men aged 20-47 years, comprising 50 active male smokers and 50 non-smokers, were randomly recruited into this comparative cross-sectional study. The PEFR was measured using a peak flow meter, serum levels of cotinine, FSH, LH, TST, TNF-α, and urine 8-OHdG by enzyme-linked immunosorbent assay and 1-HOP by high-performance liquid chromatography. Data analysis was done using a t-test and correlation analysis at p≤0.05. Results: Smokers had significantly higher cotinine (49.73±31.76 versus 0.51±0.69 ng/ml, p≤0.001), 8-OHdG (16.34±12.10 versus 5.79±2.14 ng/ml, p≤0.001) and lower PEFR (309.20±56.05 versus 452.80±45.76 L/min, p≤0.001) and LH (5.75±2.06 versus 6.97±2.79 mIU/ml, p=0.015) compared to non-smokers. Duration of exposure to cigarette smoke correlated positively with cotinine (r=0.937, p≤0.001) and 1-HOP (r=0.813, p≤0.001) while cotinine correlated positively with 1-HOP (r=0.863, p≤0.001) only in smokers. Conclusion: Reduced lung function and luteinizing hormone and concurrent increase in oxidative DNA damage associated with exposure to cigarette smoke may suggest the involvement of PAH-induced DNA damage in the development of pulmonary and reproductive impairment in smokers. Iran University of Medical Sciences 2022-09-19 /pmc/articles/PMC9700422/ /pubmed/36447550 http://dx.doi.org/10.47176/mjiri.36.108 Text en © 2022 Iran University of Medical Sciences https://creativecommons.org/licenses/by-nc-sa/1.0/This is an open-access article distributed under the terms of the Creative Commons Attribution NonCommercial-ShareAlike 1.0 License (CC BY-NC-SA 1.0), which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.
spellingShingle Original Article
Nsonwu-Anyanwu, Augusta Chinyere
Egom, Ofem Ukwetan
Eworo, Raymond Ekong
Nsonwu, Magnus Chinonye
Aniekpon, Uyime Fabian
Ekpo, Daniel Orok
Opara Usoro, Chinyere Adanna
Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers
title Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers
title_full Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers
title_fullStr Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers
title_full_unstemmed Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers
title_short Risk of Pulmonary-Reproductive Dysfunctions, Inflammation and Oxidative DNA Damage in Exposure to Polycyclic Aromatic Hydrocarbon in Cigarette Smokers
title_sort risk of pulmonary-reproductive dysfunctions, inflammation and oxidative dna damage in exposure to polycyclic aromatic hydrocarbon in cigarette smokers
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9700422/
https://www.ncbi.nlm.nih.gov/pubmed/36447550
http://dx.doi.org/10.47176/mjiri.36.108
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