| Registro completo |
| Provedor de dados: |
Genet. Mol. Biol.
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| País: |
Brazil
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| Título: |
Combined GSTM1 and GSTT1 null genotypes are strong risk factors for atherogenesis in a Serbian population
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| Autores: |
Grubisa,Ivana
Otasevic,Petar
Vucinic,Nada
Milicic,Biljana
Jozic,Tanja
Krstic,Slobodan
Milasin,Jelena
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| Data: |
2018-03-01
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| Ano: |
2018
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| Palavras-chave: |
Atherosclerosis
Gene polymorphisms
Glutathione S-transferases
Oxidative stress
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| Resumo: |
Abstract Oxidative stress (OS) plays an important role in atherogenesis and since glutathione S-transferases (GSTs) provide protection against OS, we have tested the hypothesis that deletion polymorphisms in two GSTs (GSTM1 and GSTT1) may affect the risk of developing atherosclerosis. A total of 382 individuals (200 patients with atherosclerosis and 182 healthy controls) were included in this association study. Genomic DNA was isolated from peripheral blood cells or from buccal epithelial cells and genotyping was performed using multiplex-PCR or real-time PCR methods. GSTM1 null genotype was significantly more frequent in atherosclerotic patients than in controls (52.0% vs 34.1%) and individuals with the GSTM1 null genotype had an approximately 2-fold increase in atherosclerosis risk (OR: 2.1, 95%CI=1.39-3.17, P=0.0004). GSTT1 null genotype alone did not show a statistically significant effect on atherosclerosis risk modulation, but the association approached significance (OR: 1.57, 95%CI=0.94-2.64, P=0.08). The combined analysis showed that the presence of both genes had a protective effect against atherosclerosis (OR=0.55, 95%CI=0.37-0.83, P=0.005) while double null genotypes led to a robust atherosclerosis risk increase (OR: 8.14, 95%CI= 2.41-27.51, P < 0.0001). This study demonstrated that the GSTM1 null and combined GSTM1/GSTT1 null genotypes are susceptibility factors for development of atherosclerosis in a Serbian population.
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| Tipo: |
Info:eu-repo/semantics/article
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| Idioma: |
Inglês
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| Identificador: |
http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1415-47572018000100035
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| Editor: |
Sociedade Brasileira de Genética
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| Relação: |
10.1590/1678-4685-gmb-2017-0034
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| Formato: |
text/html
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| Fonte: |
Genetics and Molecular Biology v.41 n.1 2018
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| Direitos: |
info:eu-repo/semantics/openAccess
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