Disease relevance of methylhydrazine

• Methylhydrazine, in contrast, induced selective association of oxidized beta-globin chains with the membrane skeleton and produced rigid but hyperstable membranes, features that mimicked those of RBCs in severe alpha-thalassemia [1].
• To identify the reactive part of the orthoquinone function of the tryptophan-derived cofactor found in methylamine dehydrogenase (MADH), we have determined the crystal structures of MADH from Thiobacillus versutus inhibited by methylhydrazine and (2,2,2-trifluoroethyl)hydrazine [2].
• Acute exposure to monomethylhydrazine and dinitrogen tetroxide, the principal toxic irritants in rocket fuels, is described with particular attention to the development of pulmonary edema as a herbinger of more severe central nervous system toxicity [3].
• Exposure to monomethylhydrazine (MMH), a common rocket propellant, can cause dose-related central nervous system (CNS) disturbances ranging from tremors to tonic-clonic convulsions to death [4].
• Under continuous flow operation, Rhodococcus sp. degraded the methylhydrazine content of the wastewater from a concentration of 10 to 2.5 mg/mL within 12 days and the hydrazine from approximately 0.8 to 0.1 mg/mL in 7 days [5].

Psychiatry related information on methylhydrazine

• Effects of brain surgery and EEG operant conditioning on seizure latency following monomethylhydrazine intoxication in the cat [6].
• Results of the MMH trial revealed that animals with dentate and ventrobasal thalamic lesions showed elevated seizure thresholds and slow wave sleep times relative to their own pre-lesion EEG baselines and to the pre- and post-lesion baselines of control animals [7].

High impact information on methylhydrazine

• Metabolism and activation of 1,1-dimethylhydrazine and methylhydrazine, two products of nitrosodimethylamine reductive biotransformation, in rats [8].
• Nitrosodimethylamine (DMN) and two of its metabolites, methylhydrazine (MH) and 1,1-dimethylhydrazine (UDMH), were metabolized to CO2 by liver slices obtained from Sprague-Dawley rats [8].
• Active-site structure of the soluble quinoprotein glucose dehydrogenase complexed with methylhydrazine: a covalent cofactor-inhibitor complex [9].
• Based on the results obtained in the cytotoxicity assays we also investigated the transforming potential of procarbazine (PCZ) and methylhydrazine (MeH) activated by horseradish peroxidase (HRP) using the Myc 9E cell line, which aims at the activation of a second cooperating oncogene [10].
• The inhibition constants calculated from the slow-binding inhibition kinetics are 2.2 microM for methylhydrazine and 0.3 microM for (3-hydroxybenzyl)hydrazine [11].

Chemical compound and disease context of methylhydrazine

• The Achromobacter sp. was equally efficient in degrading the organics present in the wastewater, reducing the concentration of the methylhydrazine from 10 to approximately 5 mg/mL within 12 days and that of the hydrazine from approximately 0.8 to 0.2 mg/mL in 7 days [5].
• While the Achromobacter sp. showed a preference for the degradation of the citric acid, the Rhodococcus species were most effective in reducing the methylhydrazine and the reaction product [12].

Biological context of methylhydrazine

• These results suggest that the Cu(I)-peroxide complex rather than the .CH3 plays a more important role in methylhydrazine plus Cu(II)-induced DNA damage [13].
• This paper describes a method of determining the total hydrazones content based on acid hydrolysis of gyromitrin and other related hydrazones in air-dried false morel followed by derivatisation of methylhydrazine with pentafluorobenzoyl chloride [14].
• A series of novel 2,8-dialkyl-1-oxa-2,8-diazaspiro[4.5]decan-3-ones and 2,8-dimethyl-1,2,8-triazaspiro[4.5]-decan-3-one (13), related to M1 muscarinic agonists YM796 and RS86, were synthesized by using Michael addition reaction of hydroxyurea or methylhydrazine to alpha, beta-unsaturated esters followed by cyclization reaction [15].
• Azoprocarbazine (AZO) and monomethylhydrazine (MMH) inhibited selectively the deamination of benzylamine by SSAO, when compared with their effects on MAO activities [16].
• Several metabolites of gyromitrin can produce enzyme activation ith subsequent synthesis of methylhydrazine [17].

Anatomical context of methylhydrazine

• Oxidation of methylhydrazine (MeH), dimethylhydrazine (DMH), phenylethylhydrazine or procarbazine by neutrophils from rat peritoneal exudates led to the formation of alkyl radicals [18].
• By perfusing the SSAO substrate, benzylamine, through the isolated mesenteric arterial bed of the rat, it was found that pretreatment of animals with procarbazine or monomethylhydrazine reduced metabolism of this amine by a similar degree as had been determined ex-vivo in blood vessel homogenates [19].
• Distribution characteristics of methyl-hydrazine in the plasma and cerebrospinal fluid of monkeys [20].
• Histology of rat placentas treated with methylhydrazine Ro 4-6467 [21].
• A Lumped parameter mathmatical model including extracellular fluid, intracellular fluid, and cerebrospinal fluid compartments has been applied to describe methylhydrazine (MMH) distribution kinetics in the blood and cerebrospinal fluid of Rhesus monkeys [20].

Associations of methylhydrazine with other chemical compounds

• Slow-binding inhibition does not appear to be the result of a significant enzyme conformational change because there is no change in the tryptophan fluorescence of GABA-AT upon binding either methylhydrazine or 3-hydrazinopropionate [11].
• DNA damage induced by methylhydrazines (monomethylhydrazine, 1,1-dimethylhydrazine, and 1,2-dimethylhydrazine) in the presence of metal ions was investigated by a DNA sequencing technique [13].
• Gas chromatography-mass spectrometry determination of the pentafluorobenzoyl derivative of methylhydrazine in false morel (Gyromitra esculenta) as a monitor for the content of the toxin gyromitrin [14].
• In contrast, the free radical spin trap agent dimethylpyrrolidin-N-oxide effectively inhibited PH-mediated DNA damage, while the free radical scavenger N-acetylcysteine also showed a protective effect against PH-, PZ-, HD-, HY-, and MH-mediated DNA strand scission [22].
• The DNA-iron(III) complex isolated by column chromatography was shown to catalyze the oxidation of both 2-phenylethylhydrazine and methylhydrazine by spin-trapping experiments with alpha-(4-pyridyl 1-oxide)-N-tert-butylnitrone (POBN) [23].

Gene context of methylhydrazine

• However, hepatic MAO-B activity was potentiated significantly in rats receiving methylhydrazine and both drugs caused a dose-dependent potentiation of MAO-A in homogenates of brown adipose tissue [24].
• In a parallel in-vitro study, monomethylhydrazine was without effect on MAO A in brown adipose tissue homogenates [19].
• Only 1 PLP/enzyme dimer reacted with methylhydrazine or (3-hydroxybenzyl)hydrazine, as indicated by Scatchard plots, or with 3-hydrazinopropionate, as shown by a spectrophotometric titration [11].
• Both compounds inhibited SSAO in a dose-dependent manner in all tissues examined, with methylhydrazine the more potent agent in this respect [24].

Analytical, diagnostic and therapeutic context of methylhydrazine

• Aldehydes were determined after derivatization with methylhydrazine by gas chromatography (GLC) [25].

References