Disease relevance of Monofluoressigsaures natrium

• Reaction mechanism of fluoroacetate dehalogenase from Moraxella sp. B [1].
• This has enabled biosynthetic experiments to be conducted which reveal stereochemical details on biological fluorination occurring during the biosynthesis of fluoroacetate and 4-fluorothreonine in the bacterium Streptomyces cattleya [2].
• The rumen bacterium Butyrivibrio fibrosolvens has been genetically modified to detoxify fluoroacetate (a poisonous component of trees and shrubs in Australia, Africa and Central America) and has been shown to persist when it is returned to the rumen [3].
• A pseudomonad was isolated from the fluoroacetate-producing plant Dichapetalum cymosum (Hook) Engl. and identified as Pseudomonas cepacia [4].
• Azotobacter vinelandii mutants defective for acetate utilization that were resistant to fluoroacetate (FA) were isolated [5].

Psychiatry related information on Monofluoressigsaures natrium

• Rats exposed to the selected toxic fluoroethanes showed clinical signs of fluoroacetate toxicity (lethargy, hunched posture, convulsions) [6].

High impact information on Monofluoressigsaures natrium

• The changes in pulmonary arterial blood pressure and coronary blood flow after fluoroacetate were not mediated via the autonomic nerves or adrenergic neurohumors because they still occurred after autonomic nervous system inhibition [7].
• A selective increase in myocardial blood flow also occurred in conscious dogs after fluoroacetate administration; hepatic artery flow was reduced, but other organ flows did not change significantly [7].
• Similarly, citrate stimulated ammoniagenesis in isolated mitochondria in the absence of inorganic phosphate provided that it induced L-malate exit on the citrate transporter associated with inhibition of citrate oxidation by fluoroacetate [8].
• Characterization of Arabidopsis fluoroacetate-resistant mutants reveals the principal mechanism of acetate activation for entry into the glyoxylate cycle [9].
• Purification of a fluoroacetate-specific defluorinase from mouse liver cytosol [10].

Chemical compound and disease context of Monofluoressigsaures natrium

• Isolation of an aldehyde dehydrogenase involved in the oxidation of fluoroacetaldehyde to fluoroacetate in Streptomyces cattleya [11].
• A mutant of Clostridium thermosaccharolyticum that is blocked in acetate production was isolated after treatment with nitrosoguanidine and selection for fluoroacetate resistance [12].
• The presence of carboxylesterases was established in several strains of the bacterium Helicobacter pylori employing 19F nuclear magnetic resonance spectroscopy, and the kinetic parameters of these enzymes for ethyl fluoroacetate and diethyl fluoromalonate were measured [13].
• Intracellular ATP was significantly reduced by anoxia and fluoroacetate in medium with or without glucose and by 2-DG only in substrate-free medium [14].
• In rats, hypoglycemia induced with insulin and Krebs cycle inhibition produced by fluoroacetate poisoning augmented the encephalopathic effects of octanoic acid and NH4Cl [15].

Biological context of Monofluoressigsaures natrium

• A novel pro-insecticide, 29-fluorostigmasterol, is proposed to cause mortality due to release of fluoroacetate during side chain dealkylation [16].
• FAC was significantly more effective in decreasing synaptic potentials in CA1 than in DG [17].
• FAC inhibits evoked intracellular postsynaptic potentials (PSPs; IC50 = 39 microM) as well as population PSPs (IC50 = 65 microM) in field CA1 of the guinea pig hippocampal slice [18].
• We also demonstrated no role for mitochondrial-derived radicals/respiratory chain in the lytic pathway using specific inhibitors/uncouplers (rotenone, KCN, carboxin, fluoroacetate, antimycin, malonate, carbonyl cyanide p-trifluoromethoxyphenylhydrazone) and chloramphenicol-derived respiration-deficient cells [19].
• Application of 5 mM fluoroacetate, which selectively blocks the glial Krebs cycle, suppressed rhythmic respiratory burst activity [20].

Anatomical context of Monofluoressigsaures natrium

• Since both fluoroacetate and MSO act exclusively on glial cells, the findings also show that neuronal-glial interactions are necessary during the establishment of memory [21].
• Four strains of Butyrivibrio fibrisolvens, transformed with a gene encoding fluoroacetate dehalogenase, maintained a combined population of 10(6) to 10(7) cells ml-1 in the rumens of test sheep [22].
• Fluoroacetate is known to block cell metabolism and to change potassium conductances selectively in astrocytes [23].
• Effects of fluoroacetate on the testis of the rat [24].
• (v) The lack of significant [14C]ACh synthesis from [1-14C]acetate in striatal synaptosomes is consistent with the failure of fluoroacetate to modify the amounts of 14CO2 as well as of [14C]ACh formed from [2-14C]pyruvate [25].

Associations of Monofluoressigsaures natrium with other chemical compounds

• However, the decay of both iontophoretic and evoked PSPs are prolonged following FAC treatment suggesting inhibition of glutamate uptake may contribute to the FAC-induced depression of synaptic potentials [18].
• Fluorocitrate is also detected by 19F NMR examination of fluoroacetate incubations with mouse liver cytosol [26].
• We have shown by 19F nuclear magnetic resonance (NMR) spectrometry that fluoroacetate is accumulated first in the culture broth and that accumulation of 4-fluorothreonine is next [27].
• Modulatory influences of metabolic inhibitors, such as fluoroacetate, malonate, phenylpyruvate and D-malate, as well as of L-lysine on the effects of AOA and KG also were investigated to outline metabolic processes involved in these effects [28].
• We report the first demonstration of the biotransformation of the anti-cancer drug 5-fluorouracil (FU) into two new metabolites, alpha-fluoro-beta-hydroxypropionic acid (FHPA) and fluoroacetate (FAC), in the isolated perfused rat liver (IPRL) and in the rat in vivo [29].

Gene context of Monofluoressigsaures natrium

• The Moraxella sp. strain B gene dehH1, encoding fluoroacetate dehalogenase, was placed under the control of both the GPD1 and CYC1 promoters [30].
• Selective metabolic impairment of glial cells with fluoroacetate decreased ERK activation [31].
• Fluoroacetate-resistant mutants were isolated and four different classes were identified: ack, lacking acetate kinase; pta, lacking phosphotransacetylase; facA, lacking both of these activities; and facB, which retained both of these enzyme activities [32].
• The evidence suggests that GSTZ1 may not be the major enzyme defluorinating fluoroacetate, but it does detoxify the fluoroacetate [33].
• Administration of fluoroacetate, a competitive inhibitor of aconitase activity, resulted in a dose-dependent decrease in the life span of the flies [34].

Analytical, diagnostic and therapeutic context of Monofluoressigsaures natrium

• Gas chromatography confirmed the relatively high concentrations of fluoroacetate found in toxic Gastrolobiums, a genus of indigenous Australian plants [35].
• To test the influence of these changes on the neurotoxicity of ammonia, the glial metabolic poison fluoroacetate (FA) was applied locally, through microdialysis to the hippocampal dentate gyrus [36].

References