title: Tobacco smoke induces ventricular remodeling associated with an increase in NADPH oxidase activity.
abstract: 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-γ, TNF-α and IL-10 were not different between the groups.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Internal Medicine Department, Botucatu Medical School, Univ Estadual Paulista, Botucatu, Brazil.
authors.forename: Bruna P M
authors.initials: BP
authors.lastname: Rafacho
authors.forename: Paula S
authors.initials: PS
authors.lastname: Azevedo
authors.forename: Bertha F
authors.initials: BF
authors.lastname: Polegato
authors.forename: Ana A H
authors.initials: AA
authors.lastname: Fernandes
authors.forename: Maria A
authors.initials: MA
authors.lastname: Bertoline
authors.forename: Denise C
authors.initials: DC
authors.lastname: Fernandes
authors.forename: Fernanda
authors.initials: F
authors.lastname: Chiuso-Minicucci
authors.forename: Meliza G
authors.initials: MG
authors.lastname: Roscani
authors.forename: Priscila P
authors.initials: PP
authors.lastname: Dos Santos
authors.forename: Luiz S
authors.initials: LS
authors.lastname: Matsubara
authors.forename: Beatriz B
authors.initials: BB
authors.lastname: Matsubara
authors.forename: Francisco R M
authors.initials: FR
authors.lastname: Laurindo
authors.forename: Sergio A R
authors.initials: SA
authors.lastname: Paiva
authors.forename: Leonardo A M
authors.initials: LA
authors.lastname: Zornoff
authors.forename: Marcos F
authors.initials: MF
authors.lastname: Minicucci
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006352:Heart Ventricles / Q000503:physiopathology; D007371:Interferon-gamma / Q000378:metabolism; D016753:Interleukin-10 / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism; D008297:Male; D032383:Myocytes, Cardiac / Q000502:physiology; D019255:NADPH Oxidases / Q000378:metabolism*; D018384:Oxidative Stress; D051381:Rats; D017208:Rats, Wistar; D012906:Smoke / Q000009:adverse effects*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D020257:Ventricular Remodeling / Q000502:physiology*; D014026:Nicotiana
chemical_list: D008054:Lipid Peroxides; D012906:Smoke; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D019255:NADPH Oxidases