TURKISH JOURNAL OF BIOCHEMISTRY-TURK BIYOKIMYA DERGISI, cilt.34, sa.3, ss.167-172, 2009 (SCI-Expanded)
Objectives: The reactive oxygen species and their active intermediate metabolites produced by cigarette smoke may create oxidative damage on mitochondrial DNA. Damages of mtDNA may trigger mitochondrial dysfunction. Mitochondria contribute to cardiac dysfunction and myocyte injury via a loss of metabolic capacity and by the production and release of toxic products. Reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis. These cellular events play an important role in the development and progression of maladaptive cardiac remodeling and failure. Oxidative mtDNA damage that have been created by cigarette smoke and possible protective effects of Vitamin E and selenium which are powerful antioxidants were measured in the heart tissue of Mus musculus in this study.