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Provedor de dados:  Genet. Mol. Biol.
País:  Brazil
Título:  Glutathione S-transferase mu 1 (GSTM1) and theta 1 (GSTT1) genetic polymorphisms and atopic asthma in children from Southeastern Brazil
Autores:  Lima,Carmen Silvia Passos
Néri,Iramaia Angélica
Lourenço,Gustavo Jacob
Faria,Isabel Cristina Jacinto
Ribeiro,José Dirceu
Bertuzzo,Carmen Silvia
Data:  2010-01-01
Ano:  2010
Palavras-chave:  Atopic asthma
Pathogenesis
GSTM1 gene
GSTT1 gene
Resumo:  Xenobiotics can trigger degranulation of eosinophils and mast cells. In this process, the cells release several substances leading to bronchial hyperactivity, the main feature of atopic asthma (AA). GSTM1 and GSTT1 genes encode enzymes involved in the inactivation of these compounds. Both genes are polymorphic in humans and have a null variant genotype in which both the gene and corresponding enzyme are absent. An increased risk for disease in individuals with the null GST genotypes is therefore, but this issue is controversial. The aim of this study was to investigate the influence of the GSTM1 and GSTT1 genotypes on the occurrence of AA, as well as on its clinical manifestations. Genomic DNA from 86 patients and 258 controls was analyzed by polymerase chain reaction. The frequency of the GSTM1 null genotype in patients was higher than that found in controls (60.5% versus 40.3%, p = 0.002). In individuals with the GSTM1 null genotype the risk of manifested AA was 2.3-fold higher (95%CI: 1.4-3.7) than for others. In contrast, similar frequencies of GSTT1 null and combined GSTM1 plus GSTT1 null genotypes were seen in both groups. No differences in genotype frequencies were perceived in patients stratified by age, gender, ethnic origin, and severity of the disease. These results suggest that the inherited absence of the GSTM1 metabolic pathway may alter the risk of AA in southeastern Brazilian children, although this must be confirmed by further studies with a larger cohort of patients and age-matched controls from the distinct regions of the country.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572010000300007
Editor:  Sociedade Brasileira de Genética
Relação:  10.1590/S1415-47572010000300007
Formato:  text/html
Fonte:  Genetics and Molecular Biology v.33 n.3 2010
Direitos:  info:eu-repo/semantics/openAccess
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