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Cellular and Molecular Life Sciences: CMLS logoLink to Cellular and Molecular Life Sciences: CMLS
. 2003 Jan;60(1):6–20. doi: 10.1007/s000180300001

Molecular mechanisms of N-acetylcysteine actions

M Zafarullah 1, W Q Li 1, J Sylvester 1, M Ahmad 2
PMCID: PMC11138873  PMID: 12613655

Abstract.

Oxidative stress generated by an imbalance between reactive oxygen species (ROS) and antioxidants contributes to the pathogenesis of arthritis, cancer, cardiovascular, liver and respiratory diseases. Proinflammatory cytokines and growth factors stimulate ROS production as signaling mediators. Antioxidants such as N-acetylcysteine (NAC) have been used as tools for investigating the role of ROS in numerous biological and pathological processes. NAC inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. NAC can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. NAC directly modifies the activity of several proteins by its reducing activity. Despite its nonspecificity, ability to modify DNA and multiple molecular modes of action, NAC has therapeutic value for reducing endothelial dysfunction, inflammation, fibrosis, invasion, cartilage erosion, acetaminophen detoxification and transplant prolongation.

Keywords: Key words. Free radicals; oxidative stress; antioxidants; N-acetylcysteine; cell survival; signal transduction.

Footnotes

Received 12 December 2001; received after revision 30 May 2002; accepted 18 June 2002

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