The association between glutathione S-transferase P1 polymorphisms and asthma in Egyptians

Mahmoud, Mahmoud I.; Kassem, Heba Sh.; Wahab, Nashwa Hassan Abdel; Saad, Abeer A.; Moez, Pacint

doi:10.1016/j.ajme.2011.06.008

Cited by 5 publications

(5 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Asthma is an intricate, multifactorial disease with appearance from genetic predisposition, immunological responses, and intermediate of environmental elements. It recollects as a foremost public health challenge that affects 100–150 million human beings across the globe [16]. In the current study, the incidence of bronchial asthma is higher among females than males in alignment with the earlier research [17].…”

Section: Discussionsupporting

confidence: 84%

“…An association study was designed in the literature to understand whether an allelic variation on the glutathione-S-transferase GSTP1 locus, affects the expression of BHR and atopy phenotypes in bronchial asthma. The enzyme encoded by GSTP1 makes use of a ramification of lipid and DNA products of oxidative pressure whereas the polymorphic editions of this gene are related with the enzyme’s altered catalytic function [9, 16].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Cytology and molecular study for GSTP1 effect on asthma Iraqi patients

Hamzah¹,

Shafi²,

Sharqi³

et al. 2019

Clin Mol Allergy

View full text Add to dashboard Cite

Background GST belongs to a super family of phase II detoxification enzyme and it plays an important role in preventing the damage that may occur due to reactive water-soluble compounds generated by the association of reactive intermediates with glutathione. Method In the present study, we analyzed the frequencies of GSTP1 polymorphism among the Iraqi population using PCR–RFLP technique. Fifty samples from bronchial asthma patients and fifty samples from control cases were subjected to conventional PCR and Restriction Fragment Length Polymorphism (RFLP) to detect GSTP1 genotype and measured different parameters together such as IgE, eosinophilic count, WBC, and so forth. Some of the cases were made to undergo sequence analysis and enrolled in NCBI GenBank with accession number (MG657249–MG657258). The GSTP1 polymorphism was determined using PCR and the resultant 176-bp fragment was subjected to RFLP and digested with BsamA1 to recognize the A–G transition at nucleotide. Results Homozygotes for Ile105 encoding allele resulted in 176-bp fragment found in 62% andVal105 encoding allele had two fragments of 91 and 85 bp in PCR was found in 4% of asthmatic patients. On the other hand, heterozygotes resulted in three fragments of 176, 91 and 85 bp seen in 34% of patients. Conclusion To the best of the researcher’s knowledge, this is the first-of-its-kind report with regards to the role played by GSTP1 polymorphism in bronchial asthma among the Iraqi patients. Though the study outcomes do not support the large role played by GSTP1 gene polymorphism in the evolution of bronchial asthma disorder, future researchers are suggested to investigate more features for many promising results.

show abstract

Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Cytology and molecular study for GSTP1 effect on asthma Iraqi patients

Hamzah¹,

Shafi²,

Sharqi³

et al. 2019

Clin Mol Allergy

View full text Add to dashboard Cite

show abstract

“…Due to the single nucleotide replacement of adenine (A) by guanine (G) in the GSTP1 gene, which leads to the replacement of the isoleucine amino acids (Ile105) by valine (Val105), there is a change in the enzymatic activity, which causes an increase in the level of hydrophobic adducts in lung tissue and in polycyclic aromatic hydrocarbons of the DNA adducts in blood lymphocytes. The GSTP1 polymorphism is a candidate for the development of asthmatic symptoms because it is responsible for catabolism of the lipid by-products and DNA oxidation, influencing the binding of hydrophobic electrophiles and substrate-specific catalytic activity of the enzyme [14].…”

Section: Introductionmentioning

confidence: 99%

Models of Gen-gene Interaction in Determining the Severity of Bronchial Asthma in Children

Речкіна¹,

Горовенко²,

Stryzh³

et al. 2020

AJIM

View full text Add to dashboard Cite

Bronchial asthma (BA) has a polygenic nature, and the onset of its manifestation and features course is realized due to the influence of genetic factors. This study aimed to investigate the effect of polymorphisms of the genes of the phase II detoxification system and genes of the cardiovascular tone on the severity of asthma in children. The study included 163 children aged 5-18 years: 38 with severe asthma, 69 with moderate asthma, and 56 with mild asthma. A molecular genetic study was conducted to determine the frequency of gene propagation and gen-gene interaction by GSTT1, GSTM1, GSTP1, ACE, eNOS, AT2R1, NAT2 genes at different severity of bronchial asthma. Found that in the prediction of the severity of asthma special place belongs to the analysis of the combination of genotypes. Independent effects were found for AT2R1 and ACE gene polymorphisms. The ACE (I / D) / AT2R1 (A1166C) / eNOS (T786C) / eNOS (4b / 4a) four-locus model was developed to predict the severe BA course and the need for additional analysis of the interaction of AT2R1 (A1166C) and eNOS (T786C), eNOS (T786C) genes was demonstrated (4b4a) and GSTT1. The risk of developing severe BA has been demonstrated for the combination of 1166SS + 786TT, 1166CC + 786TC genotypes by AT2R1 (A1166C) and eNOS (T786C) genes, and the reduction of this risk for combinations of eNOS (4b4a) 4b4b + GSTT1 genotypes. In moderate asthma, combinations of ACE genotypes DD + AT2R1 1166SS and AT2R1 313AA + GSTP1 1166SS were reliable risk markers for severe asthma. AT2R1 gene polymorphism was the leading marker in more severe asthma. A marker of severe BA was also found for the heterozygous 857GA polymorphism of the NAT2 gene (G857A). Conclusions. The influence of ACE (I / D), AT2R1 (A1166C), eNOS (T-786C), NAT2 (G857A), GSTT1, and GSTP1 gene polymorphisms on the severity of asthma in children has been established.

show abstract

“…This interaction result in a loss of enzyme activity, but it is essential because it protects cells from toxic substances that could interact and damage DNA and other macromolecules . However, exposure to certain air pollutants may increase oxidative stress in the epithelial tissue of the upper airways, causing inflammation of the lung tissue, because of the absence of specific detoxifying enzymes or the reduce activity of these enzymes . Through the phase I and phase II detoxification reactions, the cell is able to detoxify endogenous and exogenous toxic compounds .…”

Section: Introductionmentioning

confidence: 99%

Deletion polymorphism of GSTT1 gene as protective marker for allergic rhinitis

Iorio

Polimanti

Piacentini

et al. 2014

Clinical Respiratory J

View full text Add to dashboard Cite

Our data indicated that GSTT1 may be a susceptibility locus for AR. Specifically, the positive/null polymorphism of GSTT1 may be involved in an oxidative stress-related mechanism that may enhance pathogenic pathways related to AR. Moreover, beside GSTT1, this deletion polymorphism affects also another gene potentially related to AR phenotype, LOC391322. This gene belongs to MIF (macrophage migration inhibitory factor) gene family and several studies indicated the role of this gene in several immunology-related phenotypes. Therefore, two different scenarios may explain the observed genetic association.

show abstract

The association between glutathione S-transferase P1 polymorphisms and asthma in Egyptians

Cited by 5 publications

References 43 publications

Cytology and molecular study for GSTP1 effect on asthma Iraqi patients

Cytology and molecular study for GSTP1 effect on asthma Iraqi patients

Models of Gen-gene Interaction in Determining the Severity of Bronchial Asthma in Children

Deletion polymorphism of GSTT1 gene as protective marker for allergic rhinitis

Contact Info

Product

Resources

About