THE aim of this study was to assess whether oxidative stress induces d
eleterious NOS activity in the central nervous system (CNS). For this
purpose, the mitochondrial toxin malonate, which promotes free radical
production, was infused into the left striatum of rats. Forty-eight h
ours after injection, an increase in Ca-independent NOS activity was o
bserved in the injected striatum. This increase was blocked by alpha-p
henyl-tert-butyl-nitrone, a free radical scavenger, and by aminoguanid
ine, an inhibitor of NOS 2. Both these drugs reduced the malonate-indu
ced striatal necrotic volume. These results suggest that in the CNS ox
idative stress can induce a Ca-independent NOS, probably of type 2, wh
ich contributes to the lesion.