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Provedor de dados:  Genet. Mol. Biol.
País:  Brazil
Título:  No contribution of GSTM1 and GSTT1 null genotypes to the risk of neutropenia due to benzene exposure in Southeastern Brazil
Autores:  Lima,Carmen Silvia Passos
Lourenço,Gustavo Jacob
Lorand-Metze,Irene
Nascimento,Helvia
Saad,Sara Teresinha Ollala
Costa,Fernando Ferreira
Data:  2009-01-01
Ano:  2009
Palavras-chave:  Neutropenia
Glutathione S-transferase
GSTM1
GSTT1
Resumo:  Exposure to benzene has been associated with haematological diseases such as neutropenia (NEB) and acute myeloid leukaemia (AML). We tested whether the null genotypes of the GSTM1 and GSTT1 genes, involved in benzene inactivation, altered the risk for NEB in southeastern Brazil. Genomic DNA from 55 NEB patients and 330 controls was analysed by multiplex-polymerase chain reaction. The frequency of the GSTM1, GSTT1 and combined null genotypes was similar in patients and controls (GSTM1, 27.3% vs. 38.8%, p = 0.16; GSTT1, 25.5% vs. 19.7%, p = 0.24; GSTM1/GSTT1, 12.7% vs. 6.7%, p = 0.26; respectively). The distribution of genotype classes in NEB patients was similar to normal controls, suggesting that GSTM1 and GSTT1 null genotypes make no specific contribution to the risk of NEB. As the GSTM1 and GSTT1 null genotypes were previously associated with increased risk for AML in Brazil and elsewhere, we hypothesise that different thresholds of chemical exposure relative to distinct GSTM1 and GSTT1 genotypes may determine whether AML or NEB manifests in benzene exposed individuals from southeastern Brazil. Although indicative, our results still require support by prospective and large scale epidemiological studies, with rigorous assessment of daily chemical exposures and control of the possible contribution of other polymorphic genes involved in benzene metabolism.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572009000400006
Editor:  Sociedade Brasileira de Genética
Relação:  10.1590/S1415-47572009005000067
Formato:  text/html
Fonte:  Genetics and Molecular Biology v.32 n.4 2009
Direitos:  info:eu-repo/semantics/openAccess
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