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Safronova, O. G.; Вавилин, В. А.; Lyapunova, A. A.; Makarova, S. I.; Lyakhovich, V. V.; Казначеева, Л. Ф.; Manankin, N. A.; Batychko, O. A.; Gavalov, S. M.

doi:10.1023/a:1026001216033

Cited by 23 publications

(11 citation statements)

References 6 publications

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“…In detail, four studies were published in the 1990s, nine in the 2000s, and 21 in the last decade. Different geographical areas (and ethnicities) were not uniformly represented: 16 studies [17,18,23,24,27,[32][33][34][35][36][37][38]40,42,45,46] were performed in Eastern Asia (8 in Japan, 6 in Korea, 2 in Taiwan), nine [21,28,31,39,41,43,44,47,48] in Europe (3 in Russia, 2 in Germany, 1 in Finland, Italy, Norway, Switzerland), four [20,22,29,30] in Middle Eastern countries (3 in Turkey, 1 in Israel), two [25,26] in Southern Asia (Bangladesh, India), and one [49] in the United States of America. Another study [19] included patients from multiple Canadian and European centers.…”

Section: Resultsmentioning

confidence: 99%

Oxidative Stress and Atopic Dermatitis

et al. 2020

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Atopic dermatitis is a common chronic/chronically relapsing inflammatory skin disease, with increasing worldwide prevalence. Etiopathogenesis is complex and multifactorial, with a mix of genetic, immunological and environmental aspects. Like in other chronic inflammatory diseases, oxidative stress plays an important pathogenetic role. We reviewed in vivo research studies on humans about oxidative stress and atopic dermatitis. Although sometimes contrasting, overall, they suggest that oxidative stress may have a significant role in atopic dermatitis, but our understanding is still incomplete, at least concerning in vivo data, because of limitations of available literature. Research consists of 33 papers published in 28 years, was not always performed on large study populations, represents a limited number of countries and ethnicities—not always in proportion to their size—and is scattered over multiple papers that, in the majority of cases, cannot be pooled and/or compared because many biomarkers were studied, in different tissues and with different methods. Further, larger studies appear warranted and necessary to shed more light on this aspect of atopic dermatitis, which is important not only to improve our understanding of this disease, but also for potential clinical and therapeutic implications.

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Section: Resultsmentioning

confidence: 99%

Oxidative Stress and Atopic Dermatitis

et al. 2020

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“…Table 2 shows deviation from HWE for GSTP1 gene in four studies of relatively small size (less than 500), including three case–control studies of rather poor quality, 38 , 40 , 41 and a cohort study 42 . Only two of them 41 , 42 performed quality control of genotyping and found no genotyping error, and none of them reported blinded genotyping.…”

Section: Resultsmentioning

confidence: 99%

Glutathione-S-transferase genes and asthma phenotypes: a Human Genome Epidemiology (HuGE) systematic review and meta-analysis including unpublished data

Minelli

Granell

Newson

et al. 2009

International Journal of Epidemiology

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Background Oxidative stress is thought to be involved in the pathogenesis of asthma. Glutathione-S-transferase (GST) enzymes, which play an important role in antioxidant defences, may therefore influence asthma risk. Two common deletion polymorphisms of GSTM1 and GSTT1 genes and the GSTP1 Ile105Val polymorphism have been associated with asthma in children and adults, but results are inconsistent across studies.Methods Systematic review and meta-analysis of the effects of GST genes on asthma, wheezing and bronchial hyper-responsiveness (BHR), with inclusion of unpublished data from three studies, including the large Avon Longitudinal Study of Parents and Children (ALSPAC). Random effect or fixed effect models were used as appropriate, and sensitivity analyses were performed to assess the impact of study characteristics and quality on pooled results.Results The meta-analyses of GSTM1 (n = 22 studies) and GSTT1 (n = 19) showed increased asthma risk associated with the null genotype, but there was extreme between-study heterogeneity and publication bias and the association disappeared when meta-analysis was restricted to the largest studies. Meta-analysis of GSTP1 Ile105Val (n = 17) and asthma suggested a possible protective effect of the Val allele, but heterogeneity was extreme. Few studies evaluated wheezing and BHR and most reported no associations, although weak evidence was found for positive associations of GSTM1 null and GSTP1 Val allele with wheezing and a negative association of GSTP1 Val allele with BHR.Conclusions Our findings do not support a substantial role of GST genes alone in the development of asthma. Future studies of large size should focus on interactions of GST genes with environmental oxidative exposures and with other genes involved in antioxidant pathways. Quality of study conduct and reporting needs to be improved to increase credibility of the evidence accumulating over time.

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“…Two SNPs were located in the coding exons: rs1695 (SNP16 in this study) was located in exon 5 and rs4891 (SNP19 in this study) was located in exon 7 (table 2). Ile105Val (SNP16) was a non-synonymous substitution that has been investigated in many previous papers [11,12,13,14,15,16,17]. In addition, we sequenced the promoter region up to 3 kb upstream of exon 1, and identified 8 SNPs, 2 of which were new SNPs.…”

Section: Methodsmentioning

confidence: 99%

“…In 2000, Fryer et al [11] first reported the positive association of a single-nucleotide polymorphism [SNP; 342A→G (Ile105Val); rs1695] of GSTP1 with bronchial hyperresponsiveness, skin pick test and asthma. Subsequently, a positive association of this SNP with asthma was reported in Turkish [12, 13] and Taiwanese [14, 15] populations, and a negative association was reported in Icelandic [16] and Russian [17] populations. An association of this SNP with disease susceptibility and gene environmental interaction were also reported in childhood [15, 18] and occupational asthma [19, 20].…”

Section: Introductionmentioning

confidence: 99%

The GSTP1 Gene Is a Susceptibility Gene for Childhood Asthma and the GSTM1 Gene Is a Modifier of the GSTP1 Gene

Kamada¹,

Mashimo

Inoue

et al. 2007

Int Arch Allergy Immunol

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Background: Bronchial asthma is a chronic airway disorder characterized by bronchial inflammation. Oxidative stress is a key component of inflammation. Glutathione S-transferase P1 (GSTP1), the abundant isoform of glutathione S-transferases (GSTs) in lung epithelium, plays a key role in cellular protection against oxidative stress. Several studies have shown that the GSTP1 geneis involved in the pathogenesis of asthma and a gene-gene interaction may occur within the GST gene superfamily. Methods: We screened single-nucleotide polymorphisms (SNPs) at the GSTP1 locus and performed an association study in the Japanese population using two independent case-control groups (group 1: 391 pediatric patients with asthma, 462 adult patients with asthma, and 639 controls, and group 2: 115 pediatric patients with asthma and 184 controls). The effect of GSTM1 null/present genotype on the association between GSTP1 Ile105Val and asthma was also investigated. Results: We identified 20 SNPs at this locus and found this region consisted of one linkage disequilibrium block represented by four SNPs (tag SNPs). The association between the Ile105Val polymorphism in the GSTP1 gene and childhood asthma was significant in both groups (p = 0.047 in group 1, and p = 0.021 in group 2). This association was only significant in patients with GSTM1-positive genotype in both groups (group 1: GSTM1 present p = 0.013 and GSTM1 null p = 0.925, and group 2: GSTM1 present p = 0.015 and GSTM1 null p = 0.362). Conclusions: These findings suggest that the GSTP1 gene is a childhood asthma susceptible gene, and the GSTM1 gene is a modifier gene of GSTP1 for the risk of childhood asthma in the Japanese population.

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Cited by 23 publications

References 6 publications

Oxidative Stress and Atopic Dermatitis

Oxidative Stress and Atopic Dermatitis

Glutathione-S-transferase genes and asthma phenotypes: a Human Genome Epidemiology (HuGE) systematic review and meta-analysis including unpublished data

The <i>GSTP1</i> Gene Is a Susceptibility Gene for Childhood Asthma and the <i>GSTM1</i> Gene Is a Modifier of the <i>GSTP1</i> Gene

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