Association Between Glutathione S-Transferase M1 Polymorphism and Urinary Sodium Excretion in a Brazilian Population

Carregando...
Imagem de Miniatura
Citações na Scopus
3
Tipo de produção
article
Data de publicação
2013
Título da Revista
ISSN da Revista
Título do Volume
Editora
OXFORD UNIV PRESS
Autores
SCHREIBER, Roberto
MILL, Jose G.
NADRUZ JR., Wilson
Citação
AMERICAN JOURNAL OF HYPERTENSION, v.26, n.8, p.1024-1029, 2013
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
BACKGROUND Null genotypes of glutathione S-transferase (GST) exhibit the absence of enzymatic activity and are associated with increased cardiovascular risk. Recent reports have related both lower and higher urinary sodium excretion (USE) to higher cardiovascular risk. Here we investigate the impact of GSTM1 and GSTT1-null polymorphisms on USE in a Brazilian population. METHODS We cross-sectionally evaluated 1,308 subjects from the city of Vitoria, Brazil, based on clinical history, physical examination, anthropometry, analysis of laboratory parameters, measurement of USE, and GST polymorphisms genotyping. RESULTS The frequency of GST M1, T1, and double-deletion polymorphisms was 51%, 22%, and 11%, respectively. Individuals with the GSTM1-null genotype had lower USE than those with the non-null genotype (92.1 +/- 52.3 vs. 102.8 +/- 6 0.7 mEq/12 h; P < 0.001). Linear regression analysis adjusted for confounding factors revealed that the GSTM1-null genotype was independently associated with USE (P = 0.001). In addition, diastolic blood pressure and triglyceride levels were higher in GSTM1-null individuals than in non-null individuals in the highest tertile of USE. Finally, the presence of GSTT1-null or double-deleted genotypes did not influence USE or affect the interactions between USE and the variables studied. CONCLUSIONS Deletion of GSTM1 was associated with low USE and modulated the interaction between sodium intake and blood pressure in Brazilian subjects. These novel findings may provide a new unexplored link between sodium regulation and GST homeostasis.
Palavras-chave
GST, polymorphism, urinary sodium excretion
Referências
  1. Abu-Amero KK, 2006, BMC MED GENET, V7, DOI 10.1186/1471-2350-7-38
  2. Alderman MH, 2012, AM J HYPERTENS, V25, P727, DOI 10.1038/ajh.2012.52
  3. Beltowski J, 2008, MOL CELL BIOCHEM, V319, P163, DOI 10.1007/s11010-008-9889-z
  4. Bid HK, 2010, J POSTGRAD MED, V56, P176, DOI 10.4103/0022-3859.68633
  5. Bisi Molina Mdel C, 2003, REV SAUDE PUBL, V37, P743
  6. Bochud M, 2006, J HYPERTENS, V24, P923, DOI 10.1097/01.hjh.0000222763.84605.4a
  7. Capoluongo E, 2009, CLIN CHIM ACTA, V399, P92, DOI 10.1016/j.cca.2008.09.017
  8. Cappuccio FP, 1996, J HYPERTENS, V14, P909, DOI 10.1097/00004872-199607000-00015
  9. Cleeman JI, 2001, JAMA-J AM MED ASSOC, V285, P2486, DOI 10.1001/jama.285.19.2486
  10. Gonzalez SA, 2012, AM J HYPERTENS, V25, P620, DOI 10.1038/ajh.2012.10
  11. Habdous M, 2004, ANN BIOL CLIN-PARIS, V62, P15
  12. Hayes JD, 2000, PHARMACOLOGY, V61, P154, DOI 10.1159/000028396
  13. Hayes JD, 1995, CRIT REV BIOCHEM MOL, V30, P445, DOI 10.3109/10409239509083491
  14. Kuznetsova T, 2006, J HYPERTENS, V24, P235, DOI 10.1097/01.hjh.0000194115.89356.bd
  15. Maciel SS, 2009, ATHEROSCLEROSIS, V206, P204, DOI 10.1016/j.atherosclerosis.2009.02.011
  16. Manfredi S, 2007, MUTAT RES-FUND MOL M, V621, P106, DOI 10.1016/j.mrfmmm.2007.02.014
  17. Martin NJ, 2009, MUTAT RES-GEN TOX EN, V674, P93, DOI 10.1016/j.mrgentox.2008.09.009
  18. Mill JG, 2012, BRAZ J MED BIOL RES, V45, P799, DOI 10.1590/S0100-879X2012007500114
  19. O'Donnell MJ, 2011, JAMA-J AM MED ASSOC, V306, P2229, DOI 10.1001/jama.2011.1729
  20. Oniki K, 2008, PHARMACOGENET GENOM, V18, P275, DOI 10.1097/FPC.0b013e3282f56176
  21. Ortega RM, 2011, BRIT J NUTR, V105, P787, DOI 10.1017/S000711451000423X
  22. Pereira AC, 2001, BRAZ J MED BIOL RES, V34, P1421, DOI 10.1590/S0100-879X2001001100008
  23. Polimanti R, 2011, MOL CELL BIOCHEM, V357, P227, DOI 10.1007/s11010-011-0893-3
  24. Polimanti R, 2013, GENE, V512, P102, DOI 10.1016/j.gene.2012.09.113
  25. Sanada H, 2011, CURR HYPERTENS REP, V13, P55, DOI 10.1007/s11906-010-0167-6
  26. Stolarz-Skrzypek K, 2011, JAMA-J AM MED ASSOC, V305, P1777, DOI 10.1001/jama.2011.574
  27. Whitehead AS, 2001, CIRCULATION, V103, P7
  28. WHO MONICA Project-Principle Investigators (prepared by Tunstall Pedoe H), 1988, J CLIN EPIDEMIOL, V41, P105
  29. Wilson MH, 2003, BIOMARKERS, V8, P43, DOI 10.1080/1354750021000042439
  30. Wilson MH, 2000, FASEB J, V14, P791
  31. Yamagishi K, 2004, AM J HYPERTENS, V17, P385, DOI 10.1016/j.amjhyper.2003.12.018
  32. Zhong SL, 2006, EUR J PHARM SCI, V28, P77, DOI 10.1016/j.ejps.2006.01.002