N-acetylcysteine treatment blunts liver failure-associated impairment of locomotor activity

Abstract

Liver failure and hyperammonemia is associated with oxidative stress in brain tissue, impaired locomotor activity, cognitive deficit, permanent brain injury, coma, and death. There is no promising therapeutic option against liver failure-associated brain injury. N-acetylcysteine (NAC) acts as an antioxidant and is a source of thiol groups. This study aimed to evaluate the effect of NAC supplementation on liver failure-associated locomotor activity impairment and oxidative stress in the brain. Mice received acetaminophen (APAP; 800mg/kg, i.p) and plasma biochemical parameters, plasma, and brain ammonia level, and animals’ locomotor activity were monitored. Moreover, brain tissue markers of oxidative stress were measured. It was found that plasma and brain ammonia was increased, and markers of liver injury were significantly elevated in the APAP-treated group. Impaired locomotor activity was also detected in APAP group. Moreover, an increase in markers of oxidative stress was evident in the brain of APAP-treated mice. It was found that NAC supplementation (50, 100, and 500mg/kg, i.p) improved animals locomotor activity, and alleviated brain tissue markers of oxidative stress. These data suggest NAC as a potential protective agent with therapeutic capability against liver failure-associated brain injury.