What is the rationale for using N-acetylcysteine (NAC) in the treatment of non-acetaminophen-related liver failure (NALF)?

A 2009 RCT study (1) involving adults with NALF (including many due to drug toxicity, HBV, and autoimmune causes) found longer transplant-free survival (not overall survival) in the treatment group, especially in those with lower grade encephalopathy, or liver failure caused by drugs or HBV. 

How NAC might work in this setting (e.g. possible effect on microcirculation or 02 delivery through interference with cytokines) is not entirely clear but a cool article (2) recently reported lower serum levels of interleukin-17 among treated patients.  Fascinating!  

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References

1.Bass S, Zook N. Intravenous acetylcysteine for indications other than acetaminophen overdose. Am J Health-Syst Pharm 2013;70:1496-1501. https://www.ncbi.nlm.nih.gov/pubmed/23943180

2. Stravitz RT, Sanyal AJ, Reisch J, et al. Effects of N-acetylcysteine on cytokines in non-acetaminophen acute liver failure: potential mechanism of improvement in transplant-free survival. Liver Int. 2013;33:1324-1331. https://utsouthwestern.pure.elsevier.com/en/publications/effects-of-n-acetylcysteine-on-cytokines-in-non-acetaminophen-acu

What is the rationale for using N-acetylcysteine (NAC) in the treatment of non-acetaminophen-related liver failure (NALF)?