Failure of  N ‐Acetylcysteine to reduce alpha amanitin toxicity | Zendy

Schneider Sandra M. | Zendy; Michelson Edward A. | Zendy; Vanscoy Gordon | Zendy

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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

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.

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