Post-stroke young rats were better protected against oxidative stress by persistently upregulating genes coping with the oxidative stress like the antioxidant zinc-binding proteinmetallothionein 1a (Mt1a) and the transcriptional regulator, Sp100. The gene encoding the thioredoxin-interacting protein (Txnip), an endogenous inhibitor of the anti-oxidant thioredoxin, was upregulated with delay in young animals, suggesting that most of oxidative events may occur during the first week post-stroke. Here, MT1A is linked to stroke disorder.