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NAC (N-acetyl-L-cysteine) Date Written 2007
Author Joe Holmes Date Revised 7-4-09

This table gives a preview of the more detailed reports below. Scroll down to the full report to see the detailed information. (Webmaster's comments)
2 NAC can delay senescence of diseased EC via hTERT activation (aging process) and transient telomere stabilization... (Telomeres are required to preserve genome integrity, chromosome stability, nuclear architecture and chromosome pairing during meiosis)
3 The current evidence of benefits of NAC for late presenters is controversial because of the poor understanding of the mechanism of late toxicity. (Suggests that NAC may contribute to liver problems and to use with caution)


1. Wikipedia "Acetylcysteine (rINN; pronounced /?æs?t?l's?sti?n, ??s?t?l's?sti?n/), also known as N-acetylcysteine or N-acetyl-L-cysteine (abbreviated NAC), is a pharmaceutical drug used mainly as a mucolytic agent and in the management of paracetamol (acetaminophen) overdose." (1)

2. "Chronic treatment with N-acetyl-cystein delays cellular senescence in endothelial cells isolated from a subgroup of atherosclerotic patients. Voghel G, Thorin-Trescases N, Farhat N, Mamarbachi AM, Villeneuve L, Fortier A, Perrault LP, Carrier M, Thorin E. Department of Surgery, Research Center, Montreal Heart Institute, Faculty of Medicine, Université de Montréal, Montréal, Québec, Canada.

Endothelial senescence may contribute to the pathogenesis of age-related vascular disorders. Furthermore, chronic exposure to risk factors for cardiovascular disease (CVD) accelerates the effects of chronological aging by generating stress-dependent damages, including oxidative stress, therefore promoting stress-induced premature senescence. Our objective was to determine whether a chronic treatment with an antioxidant (N-acetyl-cystein, NAC) could delay senescence of endothelial cells (EC) isolated and cultured from arterial segments of patients with severe coronary artery disease. If EC were considered as one population (n=26), chronic NAC treatment slightly shortened telomere attrition rate associated with senescence but did not significantly delay the onset of endothelial senescence. However, in a subgroup of NAC-treated EC (n=15) cellular senescence was significantly delayed, NAC decreased lipid peroxidation (HNE), activated the catalytic subunit of telomerase (hTERT) and inhibited telomere attrition. In contrast, in another subgroup of EC (n=11) characterized by initial short telomeres, no effect of NAC on HNE and high levels of DNA damages, the antioxidant was not beneficial on senescence, suggesting an irreversible stress-dependent damage. In conclusion, chronic exposure to NAC can delay senescence of diseased EC via hTERT activation and transient telomere stabilization, unless oxidative stress-associated cell damage has become irreversible." PMID: 18302967 (2)

3. "Prolonged N-acetylcysteine therapy in late acetaminophen poisoning associated with acute liver failure - a need to be more cautious? Athuraliya TN, Jones AL. Department of Clinical Pharmacology and Clinical Toxicology, School of Medicine and Public Health, Faculty of Health, University of Newcastle, Callaghan Drive, Newcastle, NSW 2308, Australia.

ABSTRACT: Since the 1970s, N-acetylcysteine (NAC) has shown proven efficacy as an antidote for acetaminophen (APAP) poisoning and APAP-induced liver failure for early presenters. The current evidence of benefits of NAC for late presenters is controversial because of the poor understanding of the mechanism of late toxicity. In the previous issue of Critical Care, Yang and colleagues use a mouse model to demonstrate that NAC in doses similar to those used therapeutically to treat APAP poisoning in humans impairs liver regenerative capacity and that the effect is more pronounced when administered for a longer duration. Studies based on cell cultures support this evidence. Cytokine and growth factor signalling pathways are recognised to be involved in the process of liver regeneration and apoptosis. This research paper generates several issues related to the future management of APAP-induced liver failure and research into the mechanism of toxicity, especially of late toxicity." PMID: 19490595 (3)

2 PMID: 17235423
2 PMID: 18302967
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