Disease relevance of Amanita

• Marked activity of cobalt-activated acylase was found in the sera of 33 of 37 patients with acute toxic hepatitis due to poisoning with either amanita mushrooms or chemicals [1].
• We now report 6 Amanita mushroom poisonings with favorable outcome and 2 fatal acetaminophen poisonings in which the same markers were observed [2].
• The clinical features and management of nine cases of mushroom poisoning due to Amanita pantherina (eight cases) and Amanita muscaria (one case) admitted to a children's hospital are described [3].
• Upon simultaneous administration lysine-orotate increases (about 40-fold) the toxicity in mice of a crude Amanita phalloides extract [4].
• The most common etiologies are acute viral hepatitis A and B, medication overdose (e.g., acetaminophen), idiosyncratic drug reactions, ingestion of other toxins (e.g., amanita mushroom poisoning), and metabolic disorders (e.g., Reye's syndrome) [5].

High impact information on Amanita

• Within 1 hr of exposure to phalloidin, a bicyclic heptapeptide isolated from the mushroom Amanita pahlloides, at 50 micrograms/ml, 60--70% of the cells were dead (trypan blue stainable) [6].
• Also reviewed are mescaline-containing cacti, psilocybin/psilocin-containing mushrooms, and the Amanita muscaria and Amanita pantherina mushrooms that contain muscimol and ibotenic acid [7].
• Pooled data from case record studies involving 452 patients with Amanita phalloides poisoning show a highly significant difference in mortality in favour of silibinin [the main isomer contained in silymarin] (mortality 9.8% vs 18.3% with standard treatment; p < 0.01) [8].
• A novel toxic cyclopeptide from Amanita suballiacea (Murr.) mushrooms that possesses structural features similar to viroidin is described [9].
• Phalloidin, a bicyclic peptide from the poisonous Amanita phalloides mushroom, stimulates the viscosimetrically determined polymerization of G-actin to F-actin in 0.6 m potassium iodide, a medium in which spontaneous polymerization does not occur [10].

Chemical compound and disease context of Amanita

• Lysine-orotate potentiates the toxicity of an extract of the mushroom Amanita phalloides [4].
• The most promising new medical treatment for Amanita mushroom poisoning is silibinin [11].
• Comparative study of the protective effect of an anabolic steroid. The 19-nortestosterone-phenylpropionate (19 NTPP), on liver steatosis induced by Amanita phalloides and white phosphorus in rats [12].
• Mechanism of protection with 2,4-monofurfurylidene-tetra-O-methyl sorbitol (MSF) against Amanita phalloides toxicity in mice [13].

Biological context of Amanita

• Influence of zinc, D-penicillamine and oxygen on poisoning with Amanita phalloides. Zinc accelerates liver regeneration and prevents the depletion of brain noradrenaline caused by the mushroom [14].
• Furthermore, studies are described on the atmospheric pressure ionization electrospray LC-MS detection of alpha- and beta-amanitin, toxic peptides of amanita mushrooms, in urine after solid-phase extraction on RP-18 columns [15].

Anatomical context of Amanita

• Stimulation of cell surface phospholipase A2 and prostaglandin synthesis in 3T2 mouse fibroblasts by phallolysin, a toxin from Amanita phalloides [16].

Associations of Amanita with chemical compounds

• Silibinin has been used in the treatment of Amanita phalloides poisoning [17].
• Thioctic acid in Amanita poisoning [18].
• Cimetidine protection against alpha-amanitin hepatotoxicity in mice: a potential model for the treatment of Amanita phalloides poisoning [19].
• Recent experimental evidences have been produced on the protection afforded by penicillin G in rats poisoned by Amanita phalloides extracts [20].
• We conclude that N-acetylcysteine has no clinical role in the treatment of Amanita phalloides ingestion [21].

Gene context of Amanita

• The unknown stereostructure of 2-amino-3-cyclopropylbutanoic acid 1, a novel plant growth regulator isolated from the mushroom Amanita castanopsidis Hongo, was determined to be (2S,3S)-2 through its racemic and enantioselective syntheses employing the chelate-enolate Claisen rearrangement as a key step [22].
• Degenerated oligonucleotide primers designed to flank an approximately 1.2-kb fragment of the gene encoding glyceraldehyde-3-phosphate dehydrogenase (gpd) from ascomycetes and basidiomycetes were used to amplify the corresponding gpd fragments from several species of the ectomycorrhizal fungal taxa Boletus, Amanita, and Lactarius [23].
• Because of the similarity of Amanita poisoning to other toxins affecting cytochrome P450, we investigated the use of cimetidine (as a P450 cytochrome inhibitor) as an antidote against a primary toxin of the mushroom alpha-amanitin [19].
• (2R), (1'R) and (2R), (1'S)-2-amino-3-(1,2-dicarboxyethylthio)propanoic acids from Amanita pantherina. Antagonists of N-methyl-D-aspartic acid (NMDA) receptors [24].
• The basidiolipids of Amanita virosa (eng., death cup) and Cantharellus cibarius (engl., chantarelle), of all mushroom species studied, did not bind antibodies of normal human sera [25].

Analytical, diagnostic and therapeutic context of Amanita

• The tubular transport of urate was studied in 20 children poisoned with Amanita phalloides and in control group [26].
• Successful Treatment of a Child With Fulminant Liver Failure and Coma Due to Amanita phalloides Poisoning Using Urgent Liver Transplantation [27].
• Chemotherapy of Amanita phalloides poisoning with intravenous silibinin [28].
• We report the case of a 39 year old woman with Amanita phalloides-induced FLF, admitted to our intensive care unit (ICU) and treated with MARS [29].

References