title: The oxidative response of mouse hearts is modulated by genetic background.
abstract: BACKGROUND
  Smoking plays an important role in cardiovascular diseases. However, the reasons why some individuals develop those diseases and others do not remain to be explained.
  
  
  OBJECTIVE
  This study aimed at assessing the redox profile of the heart of different mouse strains after exposure to cigarette smoke.
  
  
  METHODS
  Male mice of the Swiss (n = 10), C3H (n = 10), BALB/c (n = 10) and C57BL/6 (n = 10) strains were exposed to cigarette smoke (12 cigarettes/day), while their respective controls (n = 10) were exposed to ambient air for 60 days. After being euthanized, their heart was removed for biochemical analyses.
  
  
  RESULTS
  Although the malondialdehyde content did not increase in any of the groups, catalase activity decreased in the Swiss (p < 0.05) and BALB/c (p < 0.05) strain mice as compared with their respective control groups, while myeloperoxidase decreased in the C3H (p < 0.05) and C57BL/6 (p < 0.001) strain mice as compared with their respective control groups. The reduced glutathione content decreased in the Swiss, C3H, C57BL/6 (p < 0.05) and BALB/c (p < 0,001) strain mice as compared with their respective control groups. Regarding reduced glutathione content, an increase was observed in the Swiss strain mice (p < 0.05), while a decrease was observed in the C3H (p < 0.05) and BALB/c (p < 0.001) strain mice as compared with their respective control groups. The reduced glutathione/reduced glutathione ratio showed a reduction in the Swiss and C57BL/6 (p < 0.05) strain mice as compared with their respective control groups.
  
  
  CONCLUSIONS
  The genetic background of mice can influence the antioxidant response after exposure to cigarette smoke and seems to be a determinant factor for redox imbalance in Swiss and C57BL/6 strain mice. Understanding antioxidant responses and genetic background of C3H and BALB/c strain mice might provide important information regarding cardiac resistance to cigarette smoke.
authors.affiliation: Universidade Severino Sombra, Vassouras, RJ, Brasil.
authors.forename: Marco Aurélio
authors.initials: MA
authors.lastname: Santos-Silva
authors.forename: Akinori Cardozo
authors.initials: AC
authors.lastname: Nagato
authors.forename: Eduardo Tavares Lima
authors.initials: ET
authors.lastname: Trajano
authors.forename: Jackson Nogueira
authors.initials: JN
authors.lastname: Alves
authors.forename: Ana Carla Balthar
authors.initials: AC
authors.lastname: Bandeira
authors.forename: Luís Cristóvão
authors.initials: LC
authors.lastname: Porto
authors.forename: Frank Silva
authors.initials: FS
authors.lastname: Bezerra
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D002374:Catalase / Q000235:genetics / Q000378:metabolism*; D005978:Glutathione / Q000235:genetics / Q000378:metabolism*; D006321:Heart; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D023421:Models, Animal; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000235:genetics; D009195:Peroxidase / Q000235:genetics / Q000378:metabolism*; D011897:Random Allocation; D013045:Species Specificity; D018709:Statistics, Nonparametric; D014028:Tobacco Smoke Pollution / Q000009:adverse effects*
chemical_list: D014028:Tobacco Smoke Pollution; D002374:Catalase; D009195:Peroxidase; D005978:Glutathione