Tobacco Smoke Induces Ventricular Remodeling Associated with an Increase in NADPH Oxidase Activity

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Citações na Scopus
36
Tipo de produção
article
Data de publicação
2011
Título da Revista
ISSN da Revista
Título do Volume
Editora
KARGER
Autores
RAFACHO, Bruna P. M.
AZEVEDO, Paula S.
POLEGATO, Bertha F.
FERNANDES, Ana A. H.
CHIUSO-MINICUCCI, Fernanda
ROSCANI, Meliza G.
SANTOS, Priscila P. dos
MATSUBARA, Luiz S.
Citação
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY, v.27, n.3-4, p.305-312, 2011
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background: Recent studies have assessed the direct effects of smoking on cardiac remodeling and function. However, the mechanisms of these alterations remain unknown. The aim of this study was to investigate de role of cardiac NADPH oxidase and antioxidant enzyme system on ventricular remodeling induced by tobacco smoke. Methods: Male Wistar rats that weighed 200-230 g were divided into a control group (C) and an experimental group that was exposed to tobacco smoke for a period of two months (ETS). After the two-month exposure period, morphological, biochemical and functional analyses were performed. Results: The myocyte cross-sectional area and left ventricle end-diastolic dimension was increased 16.2% and 33.7%, respectively, in the ETS group. The interstitial collagen volume fraction was also higher in ETS group compared to the controls. In addition to these morphological changes, the ejection fraction and fractional shortening were decreased in the ETS group. Importantly, these alterations were related to augmented heart oxidative stress, which was characterized by an increase in NADPH oxidase activity, increased levels of lipid hydroperoxide and depletion of antioxidant enzymes (e.g., catalase, superoxide dismutase and glutathione peroxidase). In addition, cardiac levels of IFN-gamma, TNF-alpha and IL-10 were not different between the groups. Conclusion: Cardiac alterations that are induced by smoking are associated with increased NADPH oxidase activity, suggesting that this pathway plays a role in the ventricular remodeling induced by exposure to tobacco smoke.
Palavras-chave
Oxidative stress, Tobacco smoke exposure, Cardiac remodeling
Referências
  1. Andrews Jeannette O, 2006, Crit Care Nurs Clin North Am, V18, P63, DOI 10.1016/j.ccell.2005.10.005
  2. Zornoff LAM, 2009, ARQ BRAS CARDIOL, V92, P157, DOI 10.1590/S0066-782X2009000200013
  3. NAKAMURA W, 1974, BIOCHIM BIOPHYS ACTA, V358, P251, DOI 10.1016/0005-2744(74)90455-0
  4. Giordano FJ, 2005, J CLIN INVEST, V115, P500, DOI 10.1172/JCI200524408
  5. Yao HW, 2008, AM J PATHOL, V172, P1222, DOI 10.2353/ajpath.2008.070765
  6. Nakagami H, 2003, J MOL CELL CARDIOL, V35, P851, DOI 10.1016/S0022-2828(03)00145-7
  7. PFEFFER MA, 1990, CIRCULATION, V81, P1161
  8. Jaimes EA, 2004, ARTERIOSCL THROM VAS, V24, P1031, DOI 10.1161/01.ATV.0000127083.88549.58
  9. Zielonka J, 2005, FREE RADICAL BIO MED, V39, P853, DOI 10.1016/j.freeradbiomed.2005.05.001
  10. Lang RM, 2005, J AM SOC ECHOCARDIOG, V18, P1440, DOI 10.1016/j.echo.2005.10.005
  11. Cohn JN, 2000, J AM COLL CARDIOL, V35, P569, DOI 10.1016/S0735-1097(99)00630-0
  12. Zornoff LAM, 2006, TOXICOL SCI, V90, P259, DOI 10.1093/toxsci/kfj080
  13. Minicucci MF, 2010, CELL PHYSIOL BIOCHEM, V26, P523, DOI 10.1159/000322320
  14. Ockene IS, 1997, CIRCULATION, V96, P3243
  15. Laurindo FRM, 2008, METHOD ENZYMOL, V441, P237, DOI 10.1016/S0076-6879(08)01213-5
  16. Johar S, 2006, FASEB J, V20, P1546, DOI 10.1096/fj.05-4652fje
  17. Fernandes DC, 2007, AM J PHYSIOL-CELL PH, V292, pC413, DOI 10.1152/ajpcell.00188.2006
  18. Zhao HT, 2003, FREE RADICAL BIO MED, V34, P1359, DOI 10.1016/S0891-5849(03)00142-4
  19. Burneiko RCM, 2006, FOOD CHEM TOXICOL, V44, P1167, DOI 10.1016/j.fct.2006.01.004
  20. Droge W, 2002, PHYSIOL REV, V82, P47
  21. Wang XD, 1999, J NATL CANCER I, V91, P60, DOI 10.1093/jnci/91.1.60
  22. Orosz Z, 2007, AM J PHYSIOL-HEART C, V292, pH130, DOI 10.1152/ajpheart.00599.2006
  23. Gu LZ, 2008, EUR J HEART FAIL, V10, P1057, DOI 10.1016/j.ejheart.2008.08.009
  24. Li JM, 2002, HYPERTENSION, V40, P477, DOI 10.1161/01.HYP.0000032031.30374.32
  25. Azevedo PS, 2010, CELL PHYSIOL BIOCHEM, V26, P395, DOI 10.1159/000320563
  26. BROOKS WW, 1982, ARCH ENVIRON HEALTH, V37, P93
  27. Castardeli Edson, 2005, Arq Bras Cardiol, V84, P320, DOI 10.1590/S0066-782X2005000400009
  28. Castardeli E, 2008, MED SCI MONITOR, V14, pBR62
  29. Castardeli E, 2007, EUR J HEART FAIL, V9, P1081, DOI 10.1016/j.ejheart.2007.09.004
  30. Duarte DR, 2009, CLINICS, V64, P691, DOI 10.1590/S1807-59322009000700014
  31. GREEN CR, 1996, RECENT ADV TOBACCO S, V22, P20
  32. Ewing JF, 1995, ANAL BIOCHEM, V232, P243, DOI 10.1006/abio.1995.0014
  33. Minicucci Marcos F., 2009, Inflammation & Allergy Drug Targets, V8, P334
  34. Nabeebaccus A, 2011, HEART FAIL REV, V16, P5, DOI 10.1007/s10741-010-9186-2
  35. PAIVA SAR, 2003, ARQ BRAS CARDIOL, V18, P225
  36. Paiva SAR, 2003, AM J PHYSIOL-HEART C, V284, pH2242
  37. SHINTON R, 1989, BRIT MED J, V298, P789
  38. Stokes KY, 2007, AM J PHYSIOL-HEART C, V292, pH119, DOI 10.1152/ajpheart.01142.2006
  39. Tanus-Santos JE, 2000, EUR J PHARMACOL, V396, P33, DOI 10.1016/S0014-2999(00)00194-1
  40. Zornoff Leonardo A M, 2006, Arq Bras Cardiol, V86, P276, DOI 10.1590/S0066-782X2006000400007