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PubMed1986

Synthesis and murine tissue uptake of sodium [18F]fluoroacetate.

Fluoroacetate (FAc) is well known as the rodenticide "1080" and for its potent biochemical properties, but much less is known about its behavior in vivo. In order to study this behavior, the compound was labeled with 18F. The synthesis was accomplished in good yields (30%) from carrier-added radiofluorine gas by its conversion to [18F]tetrabutylammonium fluoride, followed by a heat-assisted halogen exchange with ethylbromoacetate. The isolated ester was rapidly and quantitatively hydrolysed with base to form [18F]FAc. preliminary studies in mice revealed relatively little soft tissue retention over the 4 h study period. However, substantial bone accumulation, indicative of defluorination, occurred to a significant degree.

Animals↗
PubMed2002

Headspace solid-phase microextraction with 1-pyrenyldiazomethane on-fibre derivatisation for analysis of fluoroacetic acid in biological samples.

A new and in part automated headspace solid-phase microextraction method for quantitative determination of the highly toxic rodenticide fluoroacetic acid (FAA) in serum and other biological samples has been developed. FAA and deuterated acetic acid (internal standard) were extracted from acidified samples by a StableFlex divinylbenzene-Carboxen on polydimethylsiloxane fibre. The acids were derivatised on the fibre in-situ with 1-pyrenyldiazomethane and detected using gas chromatography-mass spectrometry with electron impact ionisation and selected ion monitoring. The calibration curve for FAA in serum was linear over the range from 0.02 to 5 microg/ml, with limits of detection and quantification of 0.02 and 0.07 microg/ml, respectively. The method was also tested with spiked whole blood, urine, stomach contents and kidney samples. It was sufficiently reliable, reproducible and sensitive for use in routine forensic toxicology applications.

Calibration↗
PubMed1997

5-Ethynyluracil (GW776): effects on the formation of the toxic catabolites of 5-fluorouracil, fluoroacetate and fluorohydroxypropionic acid in the isolated perfused rat liver model.

We studied the effects of 5-ethynyluracil (GW776), a potent inactivator of dihydropyrimidine dehydrogenase, on the metabolism of 5-fluorouracil (5-FU), in particular with respect to formation of the toxic compounds fluoroacetate (FAC) and 2-fluoro-3-hydroxypropionic acid (FHPA), using fluorine-19 nuclear magnetic resonance and the isolated perfused rat liver model. Livers were perfused with 5-FU alone at a dose of 15 mg kg(-1) body weight or with 5-FU + GW776 at doses of 15 mg 5-FU kg(-1) body weight and 0.5 mg GW776 kg(-1) body weight injected 1 h before 5-FU. All 5-FU was metabolized in experiments with 5-FU alone whereas unmetabolized 5-FU represented 94% of the fluorinated compounds measured in experiments with 5-FU + GW776. GW776 modulated both the catabolic and the anabolic pathways of 5-FU, the most striking effect being on the degradative pathway. The amount of 5-FU catabolites decreased by a factor of 27 in the presence of GW776. The modulator led to a decrease in alpha-fluoro-beta-alanine (FBAL) formation by a factor of approximately 110, while fluoride ion formation decreased by a factor of approximately 10. By strongly lowering the metabolism of 5-FU into FBAL, GW776 circumvented the transformation of FBAL into toxic FAC and FHPA. 5-FU anabolites increased by a factor of approximately 7 in the presence of GW776. The level of free fluoronucleotides and 5-fluorouridine-5'-diphosphate sugars was increased up to fivefold. No incorporation of 5-FU into RNA could be measured in experiments with 5-FU alone whereas, although low (0.1% of 5-FU injected dose), it was detectable in experiments with 5-FU + GW776. These results suggest that GW776 may be useful for attenuating the not very common but serious cardiotoxic and/or neurotoxic side-effects of 5-FU that are probably due to FBAL metabolites.

Animals↗
PubMed1998

The anti-cancer drug 5-fluorouracil is metabolized by the isolated perfused rat liver and in rats into highly toxic fluoroacetate.

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. IPRL was perfused with solutions of pure FU at two doses, 15 or 45 mg kg(-1) body weight, and rats were injected i.p. with 180 mg of FU kg(-1) body weight. Fluorine-19 NMR analysis of perfusates from IPRL and rat urine showed the presence of the normal metabolites of FU and low amounts of FHPA (0.4% or 0.1% of injected FU in perfusates from IPRL treated with 15 or 45 mg of FU kg(-1) body weight, respectively; 0.08% of the injected FU in rat urine) and FAC (0.1% or 0.03% of injected FU in perfusates from IPRL treated with 15 or 45 mg of FU kg(-1) body weight, respectively; 0.003% of the injected FU in rat urine). IPRL was also perfused with a solution of alpha-fluoro-beta-alanine (FBAL) hydrochloride at 16.6 mg kg(-1) body weight dose equivalent to 15 mg of FU kg(-1) body weight. Low amounts of FHPA (0.2% of injected FBAL) and FAC (0.07%) were detected in perfusates, thus demonstrating that FHPA and FAC arise from FBAL catabolism. As FAC is a well-known cardiotoxic poison, and FHPA is also cardiotoxic at high doses, the cardiotoxicity of FU might stem from at least two sources. The first one, established in previous papers (Lemaire et al, 1992, 1994), is the presence in commercial solutions of FU of degradation products of FU that are metabolized into FHPA and FAC; these are formed over time in the basic medium necessary to dissolve the drug. The second, demonstrated in the present study, is the metabolism of FU itself into the same compounds.

Animals↗
PubMed2004

Characterization of Arabidopsis fluoroacetate-resistant mutants reveals the principal mechanism of acetate activation for entry into the glyoxylate cycle.

The toxic acetate analogue monofluoroacetic acid was employed to isolate Arabidopsis tDNA-tagged plants deficient in their ability to utilize or sense acetate. Several tDNA-tagged lines were isolated, including two that were determined to be allelic to an EMS-mutagenized line denoted acn1 for ac non-utilizing. Following conventions, the tDNA-tagged mutants were designated acn1-2 and acn1-3. Both mutants displayed identical behavior to acn1-1 on a variety of fluorinated and nonfluorinated organic acids, indicating that resistance was specific to fluoroacetate. Thermal asymmetric interlaced PCR identified the sites of tDNA insertion in both mutants to be within different exons in a gene, which encoded a protein containing an AMP-binding motif. Reverse transcription-PCR confirmed that the gene was not expressed in the mutants, and quantitative reverse transcription-PCR showed that the gene is expressed in imbibed seeds and increases in amount during establishment. The wild type AMP-binding protein cDNA was cloned and expressed in Escherichia coli, and the expressed protein was purified by nickel chelate chromatography. The enzyme was identified as an acyl-CoA synthetase that was more active with acetate than butyrate and was not active with fatty acids longer than C-4. The enzyme was localized to peroxisomes by enzymatic analysis of organellar fractions isolated by sucrose density gradient centrifugation. Labeling studies with [(14)C]acetate showed that acn1 seedlings, like those of the isocitrate lyase mutant icl-1 (isocitrate lyase), are compromised in carbohydrate synthesis, indicating that this enzyme is responsible for activating exogenous acetate to the coenzyme A form for entry into the glyoxylate cycle.

Acetates↗
PubMedDate not supplied

Determination of sodium fluoroacetate (Compound 1080) in biological tissues.

A sensitive gas chromatographic method was developed for the determination of sodium fluoroacetate (Compound 1080 and 1080 poison) in baits and avian tissues. The procedure involves extraction of 1080 with acetone/water (8:1) followed by derivatization with pentafluorobenzyl bromide. Cleanup of the esterified extracts was carried out using minicolumns containing Florisil and the eluates were subsequently analyzed by electron capture gas chromatography. Bait samples were initially screened by thin-layer chromatography and identity of derivatized extracts was confirmed by gas chromatography/mass spectrometry.

Animals↗
PubMedDate not supplied

GC and GC-MS determination of fluoroacetic acid and phenoxy acid herbicides via triphasal extractive pentafluorobenzylation using a polymer-bound phase-transfer catalyst.

A simple and sensitive gas chromatography and gas chromatography-mass spectrometry (GC-MS) procedure has been developed for fluoroacetic acid (FA) and phenoxy acid herbicides (PAHs) via triphasal extractive pentafluorobenzylation. The triphasal system consisted of an aqueous sample, the extraction solvent toluene containing pentafluorobenzyl bromide as the derivatization reagent, and polymer-bound tri-n-butyl-methylphosphonium bromide as a phase-transfer catalyst, FA spiked in beverages, such as orange juice and milk, was extracted as its pentafluorobenzyl (PFB) derivative under moderate conditions (i.e., at a pH value of 6.5 at 60 degrees C). The detection limits were 0.10-0.20 microgram/mL by GC with electron-capture detection (GC-ECD), and 0.42-0.50 microgram/mL by full-scan GC-MS. PAHs were also detectable in the same manner within the detection limits of 0.05-0.10 microgram/mL by GC-ECD and 0.13-0.25 microgram/mL by full-scan GC-MS. Urine and serum which both contained 2,4-dichlorophenoxyacetic acid could also be analyzed by GC-MS after the triphasal pentafluorobenzylation. The detection limit was 0.20 microgram/mL in the full-scan mode and 10 ng/mL in the selected ion monitoring mode both for the urine and serum.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1979

Anaerobic growth of Escherichia coli K12 with fumarate as terminal electron acceptor. Genetic studies with menaquinone and fluoroacetate-resistant mutants.

Fifteen independent menaquinone biosynthesis mutants (men) of Escherichia coli K12, selected for their inability to use fumarate as terminal electron acceptor, were investigated. Two nutritionally distinct groups were detected. The major group (13 mutants) responded to 1,4-dihydroxy-2-naphthoate (DHN), 2-succinylbenzoate (SB) and its dilactone, whereas the minor group (2 mutants) only responded to DHN. DHN was at least five times more effective than SB but it inhibited growth at concentrations greater than 10 microM. For anaerobic growth on glucose minimal medium the auxotrophs responded to much lower concentrations of DHN and SB and these intermediates could be replaced by uracil. Anaerobic growth tests showed that glycerol, formate and H2 are good substrates for E. coli when fumarate is the ultimate electron acceptor but growth with lactate or with fumarate alone is poor. All 15 men mutations were located between glpT and purF at approximately 49 min in the E. coli linkage map. Cotransduction frequencies with relevant markers were: nalA (21%), glpT (35%) and purF (15%). The presence of at least three genetically distinct classes (menC and menD, SB-requirers; menB, DHN-requirers) was indicated using abortive transduction as a complementation test and three-factor genetic analysis. The relative orientation nalA...menC-(D,B)...purF was indicated. 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. Some of the pta mutants and all of the facA mutants failed to grow on media containing fumarate as terminal electron acceptor or anaerobically on glucose minimal medium. All four types had genetic lesions clustered between the men and purF sites. Average cotransduction frequencies with relevant markers were: nalA (4%), men (27 to 35%) and purF (71 to 80%).

Anaerobiosis↗
PubMed1992

Isolation and characterization of new fluoroacetate resistant/acetate non-utilizing mutants of Neurospora crassa.

Sixty-two mutants of the filamentous fungus Neurospora crassa were isolated on the basis of resistance to the antimetabolite fluoroacetate. Of these, 14 were unable to use acetate as sole carbon source (acetate non-utilizers, acu) and were the subject of further genetic and biochemical analysis. These mutants fell into four complementation groups, three of which did not complement any known acu mutants. Mutants of complementation group 3 failed to complement acu-8, demonstrated similar phenotypic properties and proved to be closely linked (less than 2% recombination) but not allelic. Representatives of groups 2 and 4 were mapped to independent loci; the single representative of group 1 could not be mapped. The four complementation groups were therefore designated as genes acu-10 to acu-13 respectively. All the mutants demonstrated normal acetate-induced expression of acetyl-CoA synthetase and the unique enzymes of the glyoxylate cycle and gluconeogenesis. The nature of these mutations is therefore quite different to those reported for other fungal species. Mutant acu-11 was unable to fix labelled acetate, indicating the loss of an initial transport function; partial enzyme lesions were observed for acu-12 (acetyl-CoA hydrolase) and acu-13 (acetate-inducible NAD(+)-specific malate dehydrogenase).

Acetate-CoA Ligase↗
PubMed1997

Heptanol but not fluoroacetate prevents the propagation of spreading depression in rat hippocampal slices.

We investigated whether heptanol and other long-chain alcohols that are known to block gap junctions interfere with the generation or the propagation of spreading depression (SD). Waves of SD were triggered by micro-injection of concentrated KCl solution in stratum (s.) radiatum of CA1 of rat hippocampal tissue slices. DC-coupled recordings of extracellular potential (V0) were made at the injection and at a second site approximately 1 mm distant in st. radiatum and sometimes also in st. pyramidale. Extracellular excitatory postsynaptic potentials (fEPSPs) were evoked by stimulation of the Schaffer collateral bundle; in some experiments, antidromic population spikes were evoked by stimulation of the alveus. Bath application of 3 mM heptanol or 5 mM hexanol completely and reversibly prevented the propagation of the SD-related potential shift (delta V0) without abolishing the delta V0 at the injection site. Octanol (1 mM) had a similar but less reliably reversible effect. fEPSPs were depressed by approximately 30% by heptanol and octanol, 65% by hexanol. Antidromic population spikes were depressed by 30%. In isolated, patchclamped CA1 pyramidal neurons, heptanol partially and reversibly depressed voltage-dependent Na currents possibly explaining the slight depression of antidromic spikes and, by acting on presynaptic action potentials, also the depression of fEPSPs. Fluoroacetate (FAc), a putative selective blocker of glial metabolism, first induced multiple spike firing in response to single afferent volleys and then severely suppressed synaptic transmission (confirming earlier reports) without depressing the antidromic population spike. FAc did not inhibit SD propagation. The effect of alkyl alcohols is compatible with the idea that the opening of normally closed neuronal gap junctions is required for SD propagation. Alternative possible explanations include interference with the lipid phase of neuron membranes. The absence of SD inhibition by FAc confirms that synaptic transmission is not necessary for the propagation of SD, and it suggests that normally functioning glial cells are not essential for SD generation or propagation.

Alcohols↗
PubMed2006

Scandium-catalyzed carbon-carbon bond formations using alpha-organosulfanyl and organoselanyl-alpha-fluoroacetic acid derivatives.

The scandium-catalyzed reactions of alpha-organosulfanyl and organoselanyl-alpha-fluoroacetates 1-2, acetamides 3-4 and acetonitrile 5 with soft nucleophiles proceeded to give the products 6a-b, 7a-c, 8a-c, 9a-e in good to high yields. We also successfully performed the scandium-catalyzed intramolecular cyclization reactions and obtained the unique 5-methylene-2-oxotetrahydropyrans 16-17.

Carbon↗
PubMed2005

Ecotoxicity of sodium fluoroacetate (compound 1080) to soil organisms.

Sodium fluoroacetate (compound 1080) is applied as a vertebrate pesticide in New Zealand for control of introduced mammalian pests. Despite its widespread use, little is known about the soil ecotoxicity of 1080. Therefore, the hazard of 1080 to soil invertebrates, plants, and soil microorganisms was evaluated in a series of controlled laboratory tests. No earthworm (Eisenia fetida) mortality was reported with 1080 exposures up to 865 mg/kg soil. The lowest-observable-effect concentration and the median effect level for earthworm reproduction were 100 and 90 mg/kg soil, respectively, for cocoon production and 100 and 160 mg/kg soil, respectively, for juvenile production. Lettuce (Lactuca sativa) was more sensitive than oats (Avena sativa) to 1080. Lettuce seedling emergence and seedling shoot growth were adversely affected at a soil concentration of 7 mg/kg. The presence of 1080 in soil at concentrations up to 1 g/kg soil did not affect the ability of soil microorganisms to mineralize nitrogen. Furthermore, nitrate mineralization was not inhibited in soil treated with the urine of 1080-poisoned possums (Trichosurus vulpecula). The data collectively indicate that 1080-related effects on soil organisms occur at levels well above those that have been measured in soil (<0.1 mg/kg) following application of 1080 in baits for vertebrate pest control in New Zealand.

Animals↗
PubMed2004

Neurotoxic effects of alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA) on dogs.

In order to clarify the mechanism of the neurotoxicity of 5-FU and/or its masked compounds, we studied the effects of alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA) on the formation of vacuolar changes in the dog cerebrum, using the dosage of 3.0 mg/kg/day of FBAL-HCl (FBAL x HCl) and 0.03 mg/kg/day of FA-Na (FA x Na), respectively. These 2 compounds were selected because they are the metabolites of 5-FU claimed to be responsible for the neurotoxic effects of 5-FU and/or its masked compounds, and we wanted to confirm their effects. Tegafur-uracil mixture (UFT) was used as a positive control drug for the formation of vacuolar changes in the dog cerebrum. All compounds were orally administered daily for 3 months to beagle dogs. Each study group consisted of 3 males. Neurotoxic signs such as hyperesthesia and/or excitement, as well as convulsions, were observed in both FBAL x HCl and FA x Na groups; these toxic signs were also found in the UFT group. Slight loss of body weight gain and of food consumption was observed in the FBAL x HCl and UFT groups. Neuropathologically, vacuolar changes were detected in several areas of the dog cerebrum following administration of FBAL x HCl, FA x Na or UFT. In terms of morphology, the neuropathological effects of these 2 drugs were very similar to those induced by UFT. In conclusion, we clearly showed that FBAL is one of the main substances that cause neurotoxic signs and neuropathological changes in dogs intoxicated by 5-FU or its masked compounds. Moreover, FA might be considered to be a causative factor in addition to FBAL.

Administration, Oral↗
PubMed1986

Biosynthesis of fluorothreonine and fluoroacetic acid by the thienamycin producer, Streptomyces cattleya.

An antimetabolite, THX, was isolated from fermentation broths of the thienamycin producer, Streptomyces cattleya, when the organism was grown in the presence of a fluorine-containing substrate. THX was subsequently identified as one of the four possible stereoisomers of 4-fluorothreonine. Inorganic fluoride or any one of a number of organofluorine compounds can be used as precursors of 4-fluorothreonine. In addition, 19F NMR has provided evidence that the organism synthesizes fluoroacetate under the same fermentation conditions. The in vitro antibacterial spectrum of 4-fluorothreonine is also presented.

Animals↗
PubMed2000

Sorption of fluoroacetate (compound 1080) by Colestipol, activated charcoal and anion-exchange in resins in vitro and gastrointestinal decontamination in rats.

The sorption of sodium fluoroacetate (FA) by activated charcoal (AC) and 5 anion exchange resins (AERs) was tested in 2 simulated gastrointestinal (GI) fluids. Each sorbent was incubated with FA in a shaker-water-bath at 37 C for 24 h. Supernatant was removed and filtered, and the concentration of FA was determined by gas chromatographic detection of the dichloroaniline derivative. Under simulated gastric conditions (0.1 M HCl at approximately pH 1.5), the sorbents removed the following proportions of FA from solution: Carbosorb AC, 87 +/- 2%; cholestyramine, 28 +/- 7%; colestipol, 96 +/- 0%; Amberlite IRA-96, 70 +/- 2%; DEAE-Sephadex, 7 +/- 4%; Chitosan, 66 +/- 2%. Under simulated intestinal conditions (0.05 M sodium phosphate at approximately pH 7.4), binding was as follows: Carbosorb AC, 68 +/- 4%; cholestyramine, 53 +/- 5%; colestipol, 46 +/- 2%; AmberliteIRA-96, 10 +/- 20%; DEAE-Sephadex, 64 +/- 7%; Chitosan, 5 +/- 2%. All findings differed significantly from control, with the exception of Amberlite IRA-96 and Chitosan in phosphate buffer, and DEAE-Sephadex in HCI. In a second study, rats were given 5 mg FA/kg, and then gavaged with 2 g/kg Carbosorb AC, colestipol or bentonite. Over 4 h, the area under the curve of serum FA versus time (AUC) decreased by 39% in the rats treated with colestipol and 42% in those treated with bentonite. In contrast, Carbosorb AC did not affect the AUC,yet increased Tmax In another study, mortality was assessed 96 h after rats were orally dosed with 5 mg FA/kg followed by gavage with 2 g/kg Carbosorb AC, colestipol or water immediatey or 30 min after dosing. When the sorbents were given immediately, mortality was the same as control (75%). Surprisingiy, the 30-min delay resulted in lower mortality in colestipol-treated rats, (approximately 38%) compared to 100% in the group treated with Carbosorb AC. Before any recommendation can be made regarding the use of colestipol as a GI decontaminant, the latter findings require confirmation in an intensive care setting. The potential for synergistic effects with 2 or more sorbents also warrant investigating.

Adsorption↗
PubMed2000

[The selection of fluoroacetate-resistant mutant from E. coli MMR204 and its influence on the expression of heterologous GL-7ACA acylase].

In the cultivation of gene engineered strain of Escherichia coli on glucose medium, excretion and accumulation of acetic acid inhibit not only cell growth but also the the expression of heterologous protein. It is obvious that the desirable host strain maintaining acetate at a low level is one of the approaches to increase the production of recombinant protein. The present article deals with the selection of mutants of E. coli DP19, DP8, which grow on the medium containing pyruvate as the sole carbon source in the presence of 50 mmol/L fluoroacetic acid. It is shown that mutant DP19 is defective in its phosphotransacetylase(PTA) activity and accumulates less acetate in the medium, while DP8 is defective in acetate kinase (ACK) and accumulates similar level of acetate comparing with its parent. Using pta- mutant E. coli DP19 as host, the expression of GL-7ACA acylase gene on the recombinant plasmid pMR24 is improved, and the yield of enzyme activity in flask fermentation is about twice as much as its parent.

Acetate Kinase↗
PubMedDate not supplied

Purification and identification of rat hepatic cytosolic enzymes responsible for defluorination of methoxyflurane and fluoroacetate.

Enzymes responsible for the defluorination of methoxyflurane (MOF) and fluoroacetate (FAc) were separated and purified from rat liver cytosol. Both hepatic cytosolic enzymes with defluorination activity were labile and addition of 2-mercaptoethanol had little effect on the stability of these enzymes. Glutathione S-transferase (GT) activity of the same cytosolic fractions was stable for at least 11 days. Separation of defluorination and GT enzymatic activities on DEAE-Sephadex A-50 and reduced glutathione-affinity columns revealed that the defluorinations of MOF and FAc were primarily catalyzed by anionic proteins which also exhibited GT activity. Further identification by two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed protein bands with pl values of approximately 6.5 and 6.9 and molecular weights of approximately 20,000. However, other proteins that exhibited no GT activity also defluorinated MOF and FAc, but accounted for only 10% of the total defluorination activity present in anionic proteins. Results from a separate purification experiment using a CM-cellulose column also indicated that the enzymes responsible for defluorination coeluted with cationic GTs. Collectively, these cationic enzymes were responsible for about 20% of the recovered cytosolic defluorination activities. The results suggest that the cytosolic defluorinations of both MOF and FAc are primarily the result of a dehalogenation reaction catalyzed by one or more species of rat liver cytosolic GTs.

Animals↗
PubMedDate not supplied

Liquid chromatographic determination of sodium fluoroacetate (Compound 1080) in meat baits and formulations.

A liquid chromatographic (LC) method is described for the determination of sodium fluoroacetate in meat baits and formulations. Baits were extracted with water, ultrafiltered, partitioned into butanone, back-partitioned into dilute base, and diluted with acetonitrile. Aqueous formulations of 1080 were diluted with acetonitrile. The solutions were esterified with p-bromophenacyl bromide, using crown ether catalysis, and chromatographed on a 10 micron reverse phase column. Ultraviolet absorbance was monitored at 260 nm. Samples spiked to contain 1 mg and 10 mg 1080/100 g meat gave recoveries of 84.0-103.4%.

Animals↗