Molecular mechanisms of N-acetylcysteine actions

Zafarullah, M.; Li, W. Q.; Sylvester, J.; Ahmad, M.

doi:10.1007/s000180300001

Cited by 1,343Redox biology and oxidative stressSulfur Compounds in BiologyAntioxidant Activity and Oxidative Stress

Molecular mechanisms of N-acetylcysteine actions

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Zafarullah, M., Li, W. Q., Sylvester, J., Ahmad, M.·2003·Cellular and Molecular Life Sciences (CMLS)

DOI 10.1007/s000180300001PMC PMC11138873

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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.

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NAC has antioxidant properties.
“In the present review, we will however focus on NAC because it has antioxidant and anti-inflammatory properties, and can regulate glutamatergic neurotransmission.”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Zafarullah et al., 2003
NAC is already employed as an antioxidant and GSH precursor for GSH deficiency in many infections, genetic defects, and metabolic disorders.
“NAC is already used as antioxidant and GSH precursor to treat GSH deficiency in a wide range of infections, genetic defects, and metabolic disorder (Atkuri et al., 2007; Zafarullah et al., 2003).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Zafarullah et al., 2003

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Cyclic Strain–Induced Reactive Oxygen Species Involved in ICAM-1 Gene Induction in Endothelial Cells
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THIOL REDUCING AGENTS MODULATE INDUCED APOPTOSIS IN PORCINE ENDOTHELIAL CELLS
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Fibronectin fragment mediated cartilage chondrolysis. I. Suppression by anti-oxidants
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Induction of stromelysin gene expression by tumor necrosis factor alpha is inhibited by dexamethasone, salicylate, and N-acetylcysteine in synovial fibroblasts.
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Inhibition of Thrombin-induced Neuronal Cell Death by Recombinant Thrombomodulin and E5510, a Synthetic Thrombin Receptor Signaling Inhibitor
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BUTYLATED HYDROXYTOLUENE AND N-ACETYLCYSTEINE ATTENUATES TUMOR NECROSIS FACTOR-?? (TNF-??) SECRETION AND TNF-?? mRNA EXPRESSION IN ALVEOLAR MACROPHAGES FROM HUMAN LUNG TRANSPLANT RECIPIENTS IN VITRO
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Fibronectin fragment mediated cartilage chondrolysis. II. Reparative effects of anti-oxidants
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N-acetyl cysteine inhibits cell cycle progression in pancreatic carcinoma cells.
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Apoptosis Induced by Hydrogen Peroxide under Serum Deprivation and Its Inhibition by Antisense c-jun in F-MEL Cells
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Wilson (1999) · doi:10.1002/1529-0131(199907)42:7
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Thiol chemistry and specificity in redox signaling
Winterbourn, C. C., & Hampton, M. B. (2008) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2008.05.004 · Cited by 1,226 · see citing works
The chemistry and biological activities of N-acetylcysteine
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N-Acetylcysteine—a safe antidote for cysteine/glutathione deficiency
Atkuri, K. R., Mantovani, J. J., Herzenberg, L. A., & Herzenberg, L. A. (2007) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2007.04.005 · Cited by 721 · see citing works
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Oncogene-induced reactive oxygen species fuel hyperproliferation and DNA damage response activation
Ogrunc, M., Di Micco, R., Liontos, M., Bombardelli, L., Mione, M., Fumagalli, M., Gorgoulis, V. G., & d'Adda di Fagagna, F. (2014) · Cell Death & Differentiation · doi:10.1038/cdd.2014.16 · Cited by 328 · see citing works
Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology?
Steullet, P., Cabungcal, J. H., Monin, A., Dwir, D., O'Donnell, P., Cuenod, M., & Do, K. Q. (2016) · Schizophrenia Research · doi:10.1016/j.schres.2014.06.021 · Cited by 262 · see citing works
Measuring splanchnic amino acid metabolism in vivo using stable isotopic tracers1,2
Stoll, B., & Burrin, D. G. (2006) · Journal of Animal Science · doi:10.2527/2006.8413_supple60x · Cited by 132 · see citing works
Late N‐acetylcysteine treatment prevents the deficits induced in the offspring of dams exposed to an immune stress during gestation
Lanté, F., Meunier, J., Guiramand, J., De Jesus Ferreira, M., Cambonie, G., Aimar, R., Cohen‐Solal, C., Maurice, T., Vignes, M., & Barbanel, G. (2008) · Hippocampus · doi:10.1002/hipo.20421 · Cited by 124 · see citing works
Oxidative stress-mediated mitochondrial dysfunction facilitates mesenchymal stem cell senescence in ankylosing spondylitis
Ye, G., Xie, Z., Zeng, H., Wang, P., Li, J., Zheng, G., Wang, S., Cao, Q., Li, M., Liu, W., et al. (2020) · Cell Death & Disease · doi:10.1038/s41419-020-02993-x · Cited by 115 · see citing works
Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway
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Cellular Antioxidant Levels Influence Muscle Stem Cell Therapy
Drowley, L., Okada, M., Beckman, S., Vella, J., Keller, B., Tobita, K., & Huard, J. (2010) · Molecular Therapy · doi:10.1038/mt.2010.160 · Cited by 94 · see citing works
Sulforaphane as anticancer agent: a double-edged sword? Tricky balance between effects on tumor cells and immune cells
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Authors: Zafarullah, M., Li, W. Q., Sylvester, J., & Ahmad, M.
Affiliations: Hôpital Notre-Dame (CA)
Emory University (US)
ORCID: Ahmad, M.
Venue: Cellular and Molecular Life Sciences (CMLS)
Publisher: Springer Science and Business Media LLC
Published: 2003-01-01
Volume: 60
Issue: 1
Pages: 6-20
ISSN: 1420-682X (ISSN-L)
1420-9071
DOI: 10.1007/s000180300001
PMC: PMC11138873
OpenAlex: W2024007859
Cited by: 1,343
References: 160
Citations by year: 2026: 35 · 2025: 38 · 2024: 61 · 2023: 55 · 2022: 53 · 2021: 71 · 2020: 77 · 2019: 57 · 2018: 77 · 2017: 81 · 2016: 52 · 2015: 76 · 2014: 73 · 2013: 76 · 2012: 67
FWCI: 14.25
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Cellular and Molecular Life Sciences (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Heart, Lung, and Blood Institute (R01HL066508, R01 HL-66508-01)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Sulfur Compounds in Biology
Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords: N-acetylcysteine, reactive oxygen species, oxidative stress, antioxidants, c-Jun N-terminal kinase, p38 MAPK, NF-κB, AP-1, ERK signaling, apoptosis, S-nitrosylation, endothelial dysfunction, inflammation, fibrosis, arthritis, cartilage erosion
MeSH terms: Acetylcysteine, Animals, Antioxidants, Cell Survival, Humans, Liver, Muscle, Smooth, Vascular, Oxidation-Reduction, Signal Transduction, Free Radical Scavengers, NF-kappa B, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Mitogen-Activated Protein Kinases, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases

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Molecular mechanisms of N-acetylcysteine actions

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