2-Ethylidene-1-methylhydrazinecarboxaldehyde

100.12 g/mol

100.12

DTXSID0039225

COLORLESS LIQ

32.7 Ų

1.05 g/cm³ @ Temp: 20 °C

19.5 °C (VACUUM)

143 °C

SOL IN ACETONE, BENZENE, CARBON TETRACHLORIDE, CHLOROFORM, DIETHYL ETHER, ETHANOL, ETHYL ACETATE, METHANOL, DICHLOROMETHANE AND WATER

Very sensitive to air oxidation (starts at -25 °C); sensitive to hydrolysis by both acids and alkalis.

VERY SENSITIVE TO AIR OXIDATION; SENSITIVE TO HYDROLYSIS BY BOTH ACIDS AND ALKALIS

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

Moss MO; Mycological Res 100 (5): 513-23 (1996). A discussion concerning the production of secondary fungal metabolites.|Konno K; Food Rev Internat 11 (1): 83-107 (1995). Biologically active components of posionous mushrooms are reviewed.|Beier RC, Nigg HN; Toxicology of Naturally Occurring Chemicals in Food. In: Hui YH et al; Foodborne Disease Handbook. Vol 3. Diseases Caused by Hazardous Substances. (1994) Marcel Dekker NY, NY (1994)|Blackman JR; J Am Board Fam Pract 7 (1): 31-7 (1994). This review /assists/ the physician with a clinical approach to the diagnosis and management of toxic mushroom ingestion.|For more Special Reports (Complete) data for GYROMITRIN (25 total), please visit the HSDB record page.

ETHYLIDENE GYROMITRIN (ACETALDEHYDE-N-METHYL-N-FORMYLHYDRAZONE) IS THE MAIN POISONOUS HYDRAZINE DERIVATIVE IN THE EDIBLE MUSHROOM FALSE MOREL (GYROMITRA ESCULENTA).|N-METHYL-N-FORMYLHYDRAZONES, THE TOXIC COMPD IDENTIFIED IN THE FRUITBODIES OF THE FALSE MOREL G ESCULENTA, WERE ALSO FOUND IN THE MYCELIA GROWN FROM ISOLATED ASCOSPORES. THE AMT OF ACETALDEHYDE N-METHYL-N-FORMYLHYDRAZONE (GYROMITRIN), THE MAIN HYDRAZONE COMPD OF THE FALSE MOREL, VARIED SIGNIFICANTLY AMONG THE STRAINS STUDIED.|THE MUSHROOMS GYROMITRA GIGAS, GYROMITRA FASTIGIATA, AND GYROMITRA ESCULENTA CONTAINED MORE THAN 0.5-14.7, MORE THAN 0.5 AND 1200-6400 MG GYROMITRIN/KG SOLIDS, RESP.

THE ACUTE ORAL TOXICITY OF ETHYLIDENE GYROMITRIN WAS DETERMINED IN RABBITS, RATS AND CHICKENS. RABBITS EXCRETED AT LEAST PART OF THE ADMIN ETHYLIDENE GYROMITRIN UNCHANGED IN THE URINE.

N-METHYL-N-FORMYLHYDRAZINE, FORMED BY HYDROLYSIS FROM GYROMITRIN, LOWERS THE CYTOCHROME P450 CONCN IN LIVER MICROSOMES AFTER ITS APPLICATION TO RATS. THIS DECR CAN BE INTENSIFIED BY PRETREATMENT OF THE RATS WITH PHENOBARBITAL BUT NOT BY INDUCTION WITH 3-METHYLCHOLANTHRENE. THE CYTOCHROME P450 MEDIATED OXIDATION OF METHYLFORMYLHYDRAZINE TO A HYDROXYLAMINE DERIVATIVE AND FURTHER TO A NITROSAMIDE, IS DISCUSSED IN RELATION TO ITS IMPORTANCE FOR THE BIOLOGICAL ACTION OF THE HYDRAZINE. THIS NITROSAMIDE FORMATION MAY BE THE REASON FOR THE KNOWN HEPATOCARCINOGENICITY OF METHYLFORMYLHYDRAZINE.|@ 37 °C UNDER DIFFERENT ACIDIC CONDITIONS, MIMICKING THE MILIEU OF HUMAN STOMACH, GYROMITRIN IS CONVERTED TO METHYLHYDRAZINE, A KNOWN TUMOR INDUCER IN MICE AND HAMSTERS, THROUGH AN INTERMEDIATE, N-METHYL-N-FORMYLHYDRAZINE. METHYLHYDRAZINE IS ALSO FORMED IN THE MOUSE STOMACH AFTER ORALLY ADMIN OF GYROMITRIN.|N-methyl-N-formylhydrazine is the first active intermediate of the poison gyromitrin of the mushroom: false morel. This compound is a non-competitive inhibitor of human intestinal diamine oxidase (ID50 = 1.6 X 10( -5 ) mol/l) . This concn corresponds to less than 5 g of wet weight of mushroom/l. The diamine oxidases from 5 other sources are inhibited in a similar manner. Semicarbazide and aminoguanidine are 10-respectively 1000-fold more potent inhibitors of the human intestinal diamine oxidase. An involvement of the diamine oxidase inhibitory property of N-methyl-N-formylhydrazine in toxic and mutagenic effects of the substance is considered.|Monomethylhydrazine (MMH) and unsymmetrical dimethylhydrazine (UDMH), but not N-methyl-N-formylhydrazine (MFH), a mushroom poison, can be oxidized by the weak oxidant 6-dichlorophenolindophenol. Hydrogen peroxide is formed by this oxidation, and has been found to cause decay of DNA in aqueous solution as measured by the decr viscosity of a DNA solution the presence of the hydrazines. Furthermore, MMH and UDMH but not MFH inhibit the incorporation of (3)H-thymidine and (3)H-uridine into DNA and RNA of Ehrlich ascites carcinoma (EAC). These experiments show that MFH is an inactive compound in contrast to MMH and UDMH. Since the hydrolysis rate of MFH, to induce MMH, is low, it is concluded that MFH must be activated vivo into toxic metabolites which are ultimately responsible the known high carcinogenicity of MFH.|The hepatotoxic and cancerogenic N-methyl-N-formyl hydrazine (MFH), which is formed from the mushroom poison gyromitrin, by hydrolytic cleavage in vivo and in vitro during food processing, loses its hepatotoxicity and its influence on the renal function of rats after acetylation at the free NH2-moiety. The importance of MFH-acetylation with regard to an inhibition of microsomal conversion of MFH into a toxic nitrosamide is considered. The known genetically determined heterogeneity of the acetylation rate for hydrazine derivatives in man may explain the observed differences in sensitivity towards the mushroom toxins.

Gyromitra are considered to be edible mushrooms although their potential toxicity has been long known. They have caused numerous accidents, sometimes lethal. Historical accounts of poisoning reported and the /characteristics are described/. Knowing that gyromitrin (N-methyl-N-formyl-acetyl-hydrazone) can be converted into methylhydrazine, the /data/ suggest a relation between individual sensitivity to the mushrooms and variation of every body's ability to carry out such a conversion. Several metabolites of gyromitrin can produce enzyme activation with subsequent synthesis of methylhydrazine. The cumulative activating role of consecutive ingestion is emphasized.|Gyromitra esculenta and a few other mushrooms have caused severe poisonings and even deaths in humans. Clinical data are characterized primarily by vomiting and diarrhea, followed jaundice, convulsions and coma. Gastrointestinal disorders distinguish this poisoning. Frequent Consumption can cause hepatitis and neurological diseases. The species of concern are mainly G. esculenta and G. gigas. ... Recent advances in chromatography, biochemistry and toxicology have established that other Ascomycetes species also may prove toxic. Gyromitrin (acetaldehyde methylformylhydrazone, G) and its homologs are toxic compounds that convert in vivo into N-methyl-N-formylhydrazine (MFH), and then into N-methylhydrazine (MH). The toxicity of these chemicals, which are chiefly hepatotoxic and even carcinogenic, has been established through in vivo and in vitro experiments using animals, cell cultures and biochemical systems. ...

A CASE OF FATAL POISONING BY THE MUSHROOM GYROMITRA ESCULENTA IN 53 YR OLD WOMAN IS REPORTED. CLINICAL DATA WERE CHARACTERIZED INITIALLY BY VOMITING AND DIARRHEA, AND SUBSEQUENTLY BY HYPOTENSION, ANURIA, JAUNDICE, HEMIPLEGIA AND COMA. DEATH FOLLOWED ON THE 3RD DAY. PROMINENT PATHOLOGIC FINDINGS WERE BRAIN EDEMA, NECROSIS, FATTY DEGENERATION OF THE LIVER, NEPHROSIS, SCATTERED PETECHIAE AND SMALL HEMORRHAGES.|A CASE OF POISONING OF A 4-PERSON FAMILY BY CONSUMPTION OF THE TITLE MUSHROOMS IS DESCRIBED. GYROMITRIN WAS CONVERTED IN THE STOMACH TO METHYLHYDRAZINE WHICH CAUSED HEPATOTOXICITY. CYTOLYTIC HEPATITIS, SEIZURES, AND HEMOLYSIS OCCURRED. RECOVERY OCCURRED WITHIN 4-8 DAYS.|In the second part of this review of mushroom poisonings, the syndromes with intermediate and long lag times are discussed. They include the coprinus, phalloides, gyromitrin and the orellanus syndrome. The coprinus syndrome occurs whenever alcohol is consumed after a meal containing coprine. The lag time varies according to the amount and time of alcohol intake. It is very similar to the disulfiram syndrome which is known from the adverse therapy of alcoholism. The lag time of the phalloides syndrome varies between 7 and 24 hr. It starts with massive gastroenteritis followed by hepatopathia which can lead to hepatic coma and kidney failure. The phalloides syndrome is caused by the amatoxins of the death caps which inhibit the RNA Polymerase B in the nucleus of the liver cell. The gyromitrin syndrome exhibits also a delayed onset. The hepatotoxicity and the nephrotoxicity are less severe than in the phalloides syndrome. The first metabolite of gyromitrin monomethylhydrazine is responsible for CNS-symptoms such as delirium and convulsions. In contrast to the phalloides syndrome vomiting can be the only leading symptom in gyromitrin poisoning. The orellanus syndrome has the most delayed onset of all mushroom poisonings with 1-3 weeks. It should be thought of in all cases of kidney insufficiency of unknown origin. The orellanines damage the kidney and induce all degrees of kidney insufficiency according to the amount of ingested poison. Terminal kidney failure which requires hemodialysis treatment can occur in severe cases.|Gyromitra esculenta (Persoon ex Fries) mushrooms have been responsible for severe intoxications and even deaths. Clinical data are characterized primarily by vomiting and diarrhea, and, afterwhile, by jaundice, convulsions and coma. The species of concern are mainly G. esculenta, G. fastigiata and G. gigas; nevertheless, recent advances in chromatography, biochemistry and toxicology have established that other species within the Ascomycetes may prove also toxic. The toxins, i.e. gyromitrin (N-methyl-N-formyl-N-acetyl-hydrazone) and its higher homologs, are converted in vivo into MFH (N-methyl-N-formyl-hydrazine), then into MMH (N-Methylhydrazine). The toxicity of these latter chemicals, which are chiefly hepatotoxic and even carcinogenic, has been established through in vivo, and, in vitro experiments with monocelled cultures and biochemical systems. Considering the chemical structure and the reactivity of these natural compounds, chemical and biochemical mechanisms are suggested in order to explain their intrinsic biological activity.

Gyromitrin is not produced commercially; gyromitrin is not used commercially; no technical product containing gyromitrin is available.|The first synthesis of gyromitrin was reported in 1968... by the reaction of methylhydrazine and ethyl formate to produce N-methyl-N-formylhydrazine, which was condensed with acetaldehyde to give gyromitrin.

DETERMINATION OF THE CONTENT OF GYROMITRIN IN FRESH, DRIED OR TREATED MUSHROOMS HAS BEEN PERFORMED BY GAS CHROMATOGRAPHY WITH FLAME IONIZATION DETECTION AND IDENTIFICATION BY MASS SPECTROSCOPY; PYYSALO H, NISKANEN A; J AGRIC FOOD CHEM 25: 644 (1977).|A SENSITIVE AND RAPID METHOD IS PROPOSED FOR THE DETERMINATION OF THE TOXIC PRINCIPLES IN GYROMITRA ESCULENTA. A SUITABLE ALIQUOT OF A CRUDE EXTRACT OF THE MATERIAL UNDER EXAMINATION IS SUBJECTED TO HIGH PERFORMANCE THIN-LAYER CHROMATOGRAPHY.|THIN LAYER CHROMATOGRAPHY ON SILICA GEL WITH N-BUTANOL-ACETIC ACID-WATER AS DEVELOPING SOLVENT WAS USED FOR IDENTIFYING GYROMITRIN. THE DETECTION LIMIT WAS 10 UG.