Oxidative stress has been implicated in tissue damage from traumatic brain 
injury. Heme oxygenase-1 (HO-1) is an inducible enzyme that degrades prooxidant 
heme to radical-scavenging biliverdin/bilirubin in order to protect cells from 
oxidative stress. Although HO-1 is induced after induction of brain damage, the 
regulatory mechanism of HO-1 in the brain is still unclear. Bach1 is a 
transcriptional repressor of the HO-1 gene, and plays a critical role in tissue 
protection from oxidative stress by reperfusion injury of the myocardium. In 
this study, we examined the role of Bach1 in HO-1 regulation of the various 
brain sites by investigating the expression of Bach1 and HO-1 in brain tissues 
of mice bearing Bach1-deficient (Bach1(-/-)) or wild-type (Bach1(+/+)) genes. 
While the expression levels of Bach1 mRNA in the olfactory bulb were 
significantly higher than other brain areas, those at the cortex showed the 
lowest activity. Bach1(-/-) mice showed significantly higher HO-1 mRNA 
expression levels than Bach1(+/+) mice in all brain sites studied. Moreover, 
higher induction of HO-1 was observed around damaged tissues after cold injury 
in Bach1(-/-) than Bach1(+/+) mice. Thus, Bach1 plays an important role in 
regulating the constitutive and inducible expression levels of HO-1 in the 
brain. Although a significantly higher level of HO-1 was observed in Bach1(-/-) 
than Bach1(+/+) mice, genetic ablation of the Bach1 gene failed to show any 
tissue protective effect after cold injury was inflicted on the cortex.