Heme Oxigenase-1 (HO-1) and oxidative stress in rat heart

Low oxygen tension (hypoxia) is a potent regulator of diverse biological processes. Mammalian cells respond to hypoxia in part by increased expression of several genes that encode for tissue-specific and ubiquitous proteins. The aim of this study was to evaluate the effects of chronic exposure to low tension of oxygen (hypoxia) on the induction of heme-oxygenase-1 (HO-1) as an oxidative stress model. Adult male Wistar rats were used and subdivided randomly in two groups: A:(n=10) maintained in normoxic conditions and B: (n=10) maintained in hypoxic conditions. The animal of both groups were sacrificed after 14 days. Group A showed an evident non-specific reaction. Group B presented an increased positively of HO-1 immunoreaction. This data was confirmed by western blot analysis of protein and by the study of mRNA through rtPCR. These results suggest that myocardial adaptive response to hypoxia involves up-regulation of HO-1 in cardiac cells, indicating that this enzyme may participate in regulating vascular tone via CO and thereby contributing to the pathophysiologically important defense mechanism of the heart.