The oxidative response of mouse hearts is modulated by genetic background

Arq Bras Cardiol. 2013 Feb;100(2):157-63. doi: 10.5935/abc.20130029.
[Article in English, Portuguese]

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.

MeSH terms

  • Analysis of Variance
  • Animals
  • Catalase / genetics
  • Catalase / metabolism*
  • Glutathione / genetics
  • Glutathione / metabolism*
  • Heart
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Models, Animal
  • Myocardium / metabolism*
  • Oxidation-Reduction
  • Oxidative Stress* / genetics
  • Peroxidase / genetics
  • Peroxidase / metabolism*
  • Random Allocation
  • Species Specificity
  • Statistics, Nonparametric
  • Tobacco Smoke Pollution / adverse effects*

Substances

  • Tobacco Smoke Pollution
  • Catalase
  • Peroxidase
  • Glutathione