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Association of glutathione S-transferase polymorphisms with the severity of mustard lung
[Image: see text] Introduction: Glutathione S-transferase (GST) is one of the major detoxifiers in alveoli. Polymorphism in GST genes can influence the ability of individuals to suppress oxidative stress and inflammation. The present study was aimed to explore the hypothesis that the genetic polymor...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Tabriz University of Medical Sciences
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801537/ https://www.ncbi.nlm.nih.gov/pubmed/29435433 http://dx.doi.org/10.15171/bi.2017.30 |
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author | Dastjerdi, Arash Hajizadeh Behboudi, Hossein Kianmehr, Zahra Taravati, Ali Naghizadeh, Mohammad Mehdi Kaboudanian Ardestani, Sussan Ghazanfari, Tooba |
author_facet | Dastjerdi, Arash Hajizadeh Behboudi, Hossein Kianmehr, Zahra Taravati, Ali Naghizadeh, Mohammad Mehdi Kaboudanian Ardestani, Sussan Ghazanfari, Tooba |
author_sort | Dastjerdi, Arash Hajizadeh |
collection | PubMed |
description | [Image: see text] Introduction: Glutathione S-transferase (GST) is one of the major detoxifiers in alveoli. Polymorphism in GST genes can influence the ability of individuals to suppress oxidative stress and inflammation. The present study was aimed to explore the hypothesis that the genetic polymorphisms of GST T1, M1 and P1 are associated with the severity of the mustard lung in the sulfur mustard-exposed individuals. Methods: Blood samples were taken from 185 sulfur mustard-exposed and 57 unexposed subjects. According to the stage of the mustard lung, sulfur mustard-exposed patients were categorized in the mild/moderate and severe/very severe groups. A multiplex PCR method was conducted to identify GSTM1 and GSTT1 null genotypes. To determine the polymorphisms of GSTP1 in exon 5 (Ile105Val) and exon 6 (Ala114Val), RFLP-PCR method was performed. Results: The frequency of GSTM1 homozygous deletion was significantly higher in the severe/very severe patients compared with the mild/moderate subjects (66.3% vs. 48%, P = 0.013). The GSTM1 null genotype was associated with the severity of mustard lung (adjusted odds ratio [OR], 2.257; 95% CI, 1.219-4.180). There was no significant association between GSTT1 and GSTP1 polymorphisms with the severity of the mustard lung. Conclusion: The different distribution of GSTM1 null genotype in severe/very severe and mild/moderate groups indicated that the severity of the mustard lung might be associated with the genetic polymorphism(s). |
format | Online Article Text |
id | pubmed-5801537 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Tabriz University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-58015372018-02-12 Association of glutathione S-transferase polymorphisms with the severity of mustard lung Dastjerdi, Arash Hajizadeh Behboudi, Hossein Kianmehr, Zahra Taravati, Ali Naghizadeh, Mohammad Mehdi Kaboudanian Ardestani, Sussan Ghazanfari, Tooba Bioimpacts Original Research [Image: see text] Introduction: Glutathione S-transferase (GST) is one of the major detoxifiers in alveoli. Polymorphism in GST genes can influence the ability of individuals to suppress oxidative stress and inflammation. The present study was aimed to explore the hypothesis that the genetic polymorphisms of GST T1, M1 and P1 are associated with the severity of the mustard lung in the sulfur mustard-exposed individuals. Methods: Blood samples were taken from 185 sulfur mustard-exposed and 57 unexposed subjects. According to the stage of the mustard lung, sulfur mustard-exposed patients were categorized in the mild/moderate and severe/very severe groups. A multiplex PCR method was conducted to identify GSTM1 and GSTT1 null genotypes. To determine the polymorphisms of GSTP1 in exon 5 (Ile105Val) and exon 6 (Ala114Val), RFLP-PCR method was performed. Results: The frequency of GSTM1 homozygous deletion was significantly higher in the severe/very severe patients compared with the mild/moderate subjects (66.3% vs. 48%, P = 0.013). The GSTM1 null genotype was associated with the severity of mustard lung (adjusted odds ratio [OR], 2.257; 95% CI, 1.219-4.180). There was no significant association between GSTT1 and GSTP1 polymorphisms with the severity of the mustard lung. Conclusion: The different distribution of GSTM1 null genotype in severe/very severe and mild/moderate groups indicated that the severity of the mustard lung might be associated with the genetic polymorphism(s). Tabriz University of Medical Sciences 2017 2017-08-30 /pmc/articles/PMC5801537/ /pubmed/29435433 http://dx.doi.org/10.15171/bi.2017.30 Text en © 2017 The Author(s) This work is published by BioImpacts as an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/). Non-commercial uses of the work are permitted, provided the original work is properly cited. |
spellingShingle | Original Research Dastjerdi, Arash Hajizadeh Behboudi, Hossein Kianmehr, Zahra Taravati, Ali Naghizadeh, Mohammad Mehdi Kaboudanian Ardestani, Sussan Ghazanfari, Tooba Association of glutathione S-transferase polymorphisms with the severity of mustard lung |
title | Association of glutathione S-transferase polymorphisms with the severity of mustard lung |
title_full | Association of glutathione S-transferase polymorphisms with the severity of mustard lung |
title_fullStr | Association of glutathione S-transferase polymorphisms with the severity of mustard lung |
title_full_unstemmed | Association of glutathione S-transferase polymorphisms with the severity of mustard lung |
title_short | Association of glutathione S-transferase polymorphisms with the severity of mustard lung |
title_sort | association of glutathione s-transferase polymorphisms with the severity of mustard lung |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5801537/ https://www.ncbi.nlm.nih.gov/pubmed/29435433 http://dx.doi.org/10.15171/bi.2017.30 |
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