Failure of N-Acetylcysteine to reduce alpha amanitin toxicity
Article first published online: 11 JAN 2006
Copyright © 1992 John Wiley & Sons, Ltd.
Journal of Applied Toxicology
Volume 12, Issue 2, pages 141–142, April 1992
How to Cite
Schneider, S. M., Michelson, E. A. and Vanscoy, G. (1992), Failure of N-Acetylcysteine to reduce alpha amanitin toxicity. J. Appl. Toxicol., 12: 141–142. doi: 10.1002/jat.2550120211
- Issue published online: 11 JAN 2006
- Article first published online: 11 JAN 2006
- Manuscript Revised: 29 AUG 1991
- Manuscript Accepted: 29 AUG 1991
- Manuscript Received: 28 NOV 1990
Acetaminophen undergoes toxic conversion in the liver to a free-radical intermediary which binds to glutathione. N-Acetylcysteine acts as a glutathione precursor when natural stores are depleted, and is an effective antidote for acetaminophen overdose. Mushrooms containing amatoxins (such as Amanita phalloides) may undergo similar toxic conversion. However, in our amatoxin-poisoned mouse model, N-acetylcysteine (1.2 g kg−1) produced no change in survival or hepatic enzyme elevation compared to control animals. We conclude that N-acetylcysteine has no clinical role in the treatment of Amanita phalloides ingestion.