الفهرس 
athophysiology of oxidative stress and cellular injury in critically ill patientOnly 14 pages are availabe for public view
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Abstract
N-acetylcysteine (NAC) is one of the most extensively studied antioxidants. Many potentially beneficial and protective effects of NAC have been demonstrated in experimental endotoxic and septic conditions. As a thiol-containing compound, NAC scavenges free oxygen radicals. NAC also suppresses the activation of neutrophils and macrophages )Kharazmi et al., 1988 ), attenuates leukocyte–endothelial cell adhesion and capillary leakage (Schmidt et al., 1997), and blocks the release of tumour necrosis factor alpha and IL-8, probably by modulating gene expression of these mediators at the transcriptional level (Patterson et al., 2003). It replenishes glutathione (GSH) in states of potential insufficiency. It is used both as an antioxidant and as a detoxifying agent. It is well tolerated when administered orally and has been trialed for multiple clinical uses (Dodd et al., 2008).
N-Acetylcysteine is the standard therapy for treatment of the acetaminophen (APAP) overdose patient. The primary role of NAC in the treatment of APAP toxicity is thought to be the replacement of intracellular stores of hepatic glutathione (James et al., 2003).
Carbon tetrachloride is used as a chemical intermediate in the production of fluorocarbons and some pesticides. NAC possessed beneficial anti-oxidative effects that could attenuate the severity of liver injury treated by Carbon tetrachloride (Cai et al., 2015).
Intravenous NAC improves transplant-free survival in patients with early stage non-acetaminophen related acute liver failure (Lee et al., 2009).