We assayed redox regulatory protein, thioredoxin (TRX) and TRX mRNA in the rat brain after transient and permanent middle cerebral artery (MCA) occlusion. The immunoreactivity for TRX and TRX mRNA disappeared after MCA occlusion in the ischemic core regions. On the other hand, in the perifocal ischemic regions, TRX immunoreactivity and TRX mRNA was enhanced. In addition, in transient MCA occlusion, TRX induction was stronger in the hippocampus and more widespread in the contralateral cortex than in permanent occlusion. Moreover, the induced TRX was translocated into the cellular nucleus after ischemia and ischemia-reperfusion. These results suggest that TRX induction was accompanied with reactive oxygen intermediates (ROI) overproduction and may play an important role not only in scavenging ROI but also in signal transduction during ischemia.