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Mitochondrial oxidative stress and damage is connected to neuronal cell death and behavioral outcomes after TBI. Antioxidant treatment with the amide form of N-acetylcsyteine, which has central nervous system (CNS) bioavailability, was shown to improve markers of damage and cognitive function in rats when provided by intraperitoneal injection post experimental TBI.

Amide Form of N-acetylcysteine Improves Outcomes in Experimental TBI