Skip to main content
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

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.