The induction of heme oxygenase (HO), the rate-limiting enzyme in heme degradation, occurs as an adaptative
response to oxidative stress and is consequent to decrease in cellular glutathione levels. Our previous studies demonstrated
significant increase in survival rates of rats treated with glutathione depletors and submitted to transient cerebral ischemia.
The aim of the present research was to test the effects of L-Buthionine sulfoximine (BSO), a glutathione depletor, during
cerebral post-ischemic reperfusion. Cerebral ischemia was induced by bilateral clamping of common carotid arteries for
20 min. Each sample was used for glutathione ad lipid peroxidation level dosage and for evaluating the expression of
heme oxygenase both after a single subcutaneous administration of BSO and without treatment. In the same experimental
conditions, endothelial, inducible and neuronal Nitric Oxide Synthase (eNOS, iNOS and nNOS) and Dimethylarginine
Dimethyl amine Hydrolases (DDAH-1 and DDAH-2) were also evaluated. Results obtained in the present study suggested
that HO-1 over-expression may be implicated in the protective effect of BSO in post-ischemic reperfusion brain damage,
although the involvement of other important stress mediators cannot be ruled out.
Keywords: L-Buthionine sulfoximine, cerebral ischemia, glutathione, heme oxygenase, nitric oxide, reperfusion.
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