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Failure of N ‐Acetylcysteine to reduce alpha amanitin toxicity
Author(s) -
Schneider Sandra M.,
Michelson Edward A.,
Vanscoy Gordon
Publication year - 1992
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.2550120211
Subject(s) - amanita phalloides , acetylcysteine , antidote , amanita , acetaminophen , glutathione , toxicity , pharmacology , ingestion , chemistry , antioxidant , acetaminophen overdose , toxicology , medicine , biochemistry , enzyme , biology , botany , organic chemistry
Abstract 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.