Aim:To investigate the effects of N-acetylcysteine on D-galactosamine (Ga1N)/lipopolysaccharide (LPS)-induced apoptotic liver injury in mice.Methods:Whengiven together with a low dose of LPS,Ga1N highly sensitizes animals to produceapoptotic liver injury with severe hepatic congestion,resulting in rapid death.Inthe Ga1N/LPS model,TNF-α is the major mediator leading to apoptotic liver injury.Reactive oxygen species (ROS) are involved in Ga1N-induced sensitization toTNF-α-evoked hepatocyte apoptosis.N-acetylcysteine (NAC) is an antioxidantand a glutathione (GSH) precursor.In this study,we investigated the effects ofNAC on LPS-induced apoptotic liver injury in Ga1N-sensitized mice.Results:Pretreatment with NAC significantly reduced Ga1N/LPS-induced elevation ofserum alanine aminotransferase levels.In parallel,Ga1N/LPS-induced hepaticnecrosis and congestion were obviously improved by NAC.Furthermore,NACpretreatment significantly alleviated Ga1N/LPS-induced hepatic apoptosis,mea-sured by the inhibition of hepatic caspase-3 activity and attenuation of DNAladdering.NAC pretreatment had no effect on LPS-evoked nitric oxide productionin Ga1N-sensitized mice.Increases in serum TNF-α concentration,which wereobserved in Ga1N/LPS-treated mice,were not significantly reduced by NAC.Although NAC pretreatment significantly alleviated LPS-induced hepatic GSHdepletion,DL-buthionine-(SR)-sulfoximine,an inhibitor of GSH synthesis,did notinfluence the protective effect of NAC on Ga1N/LPS-induced apoptotic liver injury.Conclusion:NAC attenuates Ga1N/LPS-induced apoptotic liver injury via its strongROS scavenging and anti-apoptotic effects. Aim: To investigate the effects of N-acetylcysteine ​​on D-galactosamine (GaIN) / lipopolysaccharide (LPS) -induced apoptotic liver injury in mice. Methods: Whengiven together with a low dose of LPS, GaIN highly sensitizes animals to produce apoptotic liver injury with Severe hepatic congestion, resulting in rapid death. Inthe GaI N / LPS model, TNF-alpha is the major mediator leading to apoptotic liver injury. Reactive oxygen species (ROS) are involved in GaI N-induced sensitization to TNF- alpha-evoked hepatocyte apoptosis. N In this study, we investigated the effects of NAC on LPS-induced apoptotic liver injury in Ga1N-sensitized mice. Results: Pretreatment with NAC significantly reduced Ga1N / LPS-induced elevation of serum alanine aminotransferase levels. In parallel, GaI N / LPS-induced hepatic necrosis and congestion were significantly improved by NAC. Stillrther, NAC pretreatment of significantly reduced GaI / LPS-induced hepatic apoptosis, mea-sured by the inhibition of hepatic caspase-3 activity and attenuation of DNAladdering. NAC pretreatment had no effect on LPS-evoked nitric oxide production in Ga1N-sensitized mice. creases in serum TNF-α concentration, which wereobserved in Ga1N / LPS-treated mice, were not significantly reduced by NAC. Although NAC pretreatment significantly alleviated LPS-induced hepatic GSH depletion, DL-buthionine- (SR) -sulfoximine, an inhibitor of GSH synthesis, did not affect the protective effect of NAC on GaI N / LPS- induced apoptotic liver injury. Conlusion : NAC attenuates Ga1N / LPS-induced apoptotic liver injury via its strong ROS scavenging and anti-apoptotic effects.