Sodium Fluoroacetate (also known as 1080)

CAS No. 62-74-8
For more abstracts search PubMed or Toxnet

ACTIVITY: Rodenticide, Insecticide (unclassified)

CAS Name: Sodium fluoroacetate


Immediately Dangerous to Life and Health (IDLH)
Revised IDLH: 2.5 mg/m3
Original (SCP) IDLH: 5 mg/m3

Basis for revised IDLH:
No inhalation toxicity data are available on which to base an IDLH for sodium fluoroacetate. Therefore, the revised IDLH for sodium fluoroacetate is 2.5 mg/m3 based on acute oral toxicity data in humans [Deichmann and Gerarde 1969].

ACUTE TOXICITY DATA: Lethal dose data:

Species Reference Route LD50
Adjusted LD Derived value
Rat Lehman 1951 oral 1.7 12 mg/m 1.2 mg/m3
Rabbit McIlroy 1982 oral 0.34 2.4 mg/m 0.24 mg/m3
Rat Ward 1946 oral 0.1 0.7 mg/m 0.07 mg/m3
G. pig Ward 1946 oral 0.3 2.1 mg/m 0.21 mg/m3
Yakkyoku 1977 oral 0.1 0.7 mg/m 0.07 mg/m3


1. Deichmann WB, Gerarde HW [1969]. Sodium fluoroacetate (1080). In: Toxicology of drugs and chemicals. New York, NY: Academic Press, Inc., p. 542.
2. Lehman AJ [1951]. Chemicals in foods: a report to the Association of Food and drug Officials on current developments. Part II. Pesticides. Section I. Introduction. Q Bulletin Assoc Food Drug Off U.S. 15(4):122-123.
3. McIlroy JC [1982]. The sensitivity of Australian animals to 1080 poison. III. Marsupial and eutherian herbivores. Australian Wildlife Research 9:487-503.
4. Ward JC [1946]. Rodent control with 1080, ANTU, and other war-developed toxic agents. Am J Public Health Nations Health 36:1427-1431.
5. Yakkyoku (Pharmacy) [1977]; 28(3):329-339 (in Japanese).

Ref: Sodium fluoroacetate. IDHL Documentation.


Toxicol Sci. 2002 Oct;69(2):439-47.
A 90-day toxicological evaluation of Compound 1080 (sodium monofluoroacetate) in Sprague-Dawley rats.

Eason CT, Turck P.

Landcare Research New Zealand Ltd., Canterbury Agriculture & Science Center, Gerald Street, Lincoln 8152, New Zealand. easonc@landcareresearch.co.nz

Groups of Sprague-Dawley rats received sodium monofluoroacetate (Compound 1080) at 0.025, 0.075, and 0.25 mg/kg by oral gavage once daily for 90 days and were then euthanized. The control and 0.25 mg/kg/day groups included additional rats of each sex that were treated for 90 days, then maintained without treatment for a further 56-day recovery period. Microscopic changes were restricted to the testes and the heart, and were seen only in males dosed with 1080 at 0.25 mg/kg/day and included severe hypospermia in the epididymides, severe degeneration of the seminiferous tubules of the testes, and cardiomyopathy. Sperm evaluation indicated severe decreases in all three sperm parameters evaluated (concentration, % motile, and % abnormal) at 0.25 mg/kg/day. There were no microscopic changes or 1080-related effects on sperm parameters at 0.025 and 0.075 mg/kg/day. The no observable effects level (NOEL) for rats administered 1080 via oral gavage for 90 days was 0.075 mg/kg/day. The lowest observable effects level (LOEL) dose was 0.25 mg/kg/day. After dosing with the LOEL dose of 0.25 mg/kg/day, mean concentrations of 1080 in rat plasma were 0.26 micro g/ml at 1 h and 0.076 microg/ml at 12 h. Rat urine collected from the same animals contained 0.059 microg/ml.

PMID: 12377993 [PubMed - indexed for MEDLINE]

From Toxline at Toxnet

Acute toxicity of sodium monofluoroacetate to cattle.

Robison WH

J. Wildlife Management; 34(3): 647-8 1970; (REF:3)

HAPAB Abstract: Twenty-four Hereford calves (steers and heifers) and ten Hereford cows were given 0.078, 0.156, 0.312 or 0.624 mg sodium monofluoroacetate/kg body weight to determine the toxicity of the rodenticide to cattle. The sodium monofluoroacetate was encapsulated with granulated sugar in gelatin capsules and placed at the back of the animals' throats. The LD50s were calculated by the methods of Thompson (1947) and Weil (1952). There was a marked absence of detectable gross symptoms of poisoning until just before death. However, the symptoms shown by the animals were extremely consistent. The time between dosing and death varied inversely with the size of the dose. Terminal symptoms (urination followed by staggering, falling down, slight spasms, in turn followed by ,in-place running' and death) lasted from 3 to 20 min. The LD50s (95% confidence limits) were 0.393 and 0.221 mg/kg for cows and calves, respectively. Chenowith (1949) found that sheep, horse, swine and chicken (LD50 of 2.0, 1.0, less than 1.0 and 5.0 mg/kg, respectively) were less susceptible to sodium monofluoroacetate. It was concluded that sodium monofluoroacetate is extremely toxic to cattle and that when it is used in grain or in other forms of bait that cattle might ingest, precautions must be taken so that it is not available to them. 1970

CAS Registry Numbers: 62-74-8


Reports available from The National Technical Information Service (NTIS )
- see http://www.ntis.gov/
Details Abstract or Keywords

1999 - Cumulative Index to Chemicals and to Common and Scientific Names of Species Listed in Contaminant Hazard Reviews 1 Through 34.

Author: Eisler R

National Biological Service, Laurel, MD. Patuxent Wildlife Research Center.

Order Number: NTIS/01570034, 75p

Biological Science rept. The Contaminant Hazard Reviews (CHR) series-sponsored by the U.S. Geological Survey Patuxent Wildlife Research Center-synthesizes ecotoxicological data for selected environmental contaminants, with emphasis on hazards to native species of flora and fauna. From 1985 through 1998, 34 reviews were published in various report series of the U.S. Department of the Interior on agricultural pesticides (acrolein, atrazine, carbofuran, chlordane, chlorpyrifos, diazinon, diflubenzuron, famphur, fenvalerate, mirex, paraquat, toxaphene), metals and metalloids (arsenic, boron, cadmium, chromium, copper, lead, mercury, molybdenum, nickel, selenium, silver, tin, zinc), mammalian biocides (sodium monofluoroacetate), organic industrial and municipal wastes (dioxins, pentachlorophenol, polycyclic aromatic hydrocarbons, polychlorinated biphenyls), mining wastes (cyanide), and ionizing radiations. This current report is a cumulative index to the common and scientific names of all biological species listed in the first 34 reports in the CHR series, with individual species cross- referenced by contaminant and corresponding page numbers. A similar index for chemicals is included.



Order Number: NTIS/OTS0558955
Source: EPA/OTS; Doc #86970000745


CAS Registry Numbers:

1995 - Reregistration Eligibility Decision (RED): Sodium Fluoroacetate.

Environmental Protection Agency, Washington, DC. Office of Pesticide Programs.

Order Number: NTIS/PB96-112941, 92p

This document presents the Agency's decision regarding the reregistration eligibility of the registered uses of sodium fluoroacetate. Section I is the introduction. Section II describes sodium fluoroacetate, its uses, data requirements and regulatory history. Section III discusses the human health and environmental assessment based on the data available to the Agency, Section IV presents the reregistration decision for sodium fluoroacetate. Section V discusses the reregistration requirements for sodium fluoroacetate. Finally, Section VI is the Appendices which support this Reregistration Eligibility Decision.



Order Number: NTIS/OTS0572560
EPA/OTS; Doc #86950000254


CAS Registry Numbers:



Order Number: NTIS/OTS0572561
EPA/OTS; Doc #86950000255


CAS Registry Numbers:

1995 - Sodium Monofluoroacetate (1080) Hazards to Fish, Wildlife, and Invertebrates: A Synoptic Review.

Author: Eisler R

National Biological Service, Laurel, MD. Patuxent Environmental Science Center.

Order Number: NTIS/PB95-189007, 53p

Sodium monofluoroacetate (CH2FCOONa), also known as 1080, domestic use is currently restricted to livestock-protection collars on sheep and goats to selectively kill depredating coyotes. The chemical is readily absorbed by ingestion or inhalation. At lethal doses, metabolic conversion of fluoroacetate to fluorocitrate results in the accumulation of citrate in the tissues and death within 24 h from ventricular fibrillation or from respiratory failure; no antidote is available. At sublethal doses, the toxic effects of 1080 are reversible. Primary and secondary poisoning of nontarget vertebrates may accompany the use of 1080. The use of 1980 seems warranted in the absence of suitable alternative control methods. National Biological Service, Laurel, MD. Patuxent Environmental Science Center rept. no. R-30. See also PB87-116471 and PB87-182226.

Toxic hazards
Halogenated pesticides
Natural resources management
Fluorine organic compounds
Compound 1080

1991 - Mammalian wildlife (mink and ferret) toxicity test protocols (LC50, reproduction, and secondary toxicity).

Authors: Ringer RK, Hornshaw TC, Aulerich RJ

Department of Animal Science, Michigan State University, East Lansing, MI.

NTIS Technical Report (NTIS/PB91-216507) (EPA/600/3-91/043) 1991 Jul;:84 pp.

Protocols describing guidelines for conducting dietary LC50 and reproduction toxicity tests and for assessing the primary versus secondary toxicity of a test substance using carnivorous mammalian wildlife, specifically mink (Mustela vison) or European ferrets (Mustela putorius furo) are presented. These protocols go beyond the procedural steps and include the rationale behind each recommendation. In the LC50 test, test species are fed diets that contain several concentrations of a test substance for 28 days in which signs of toxicity and mortality are recorded and toxicity is expressed as the mean lethal concentration of the test substance. The reproduction protocol contains guidelines for determining the reproductive toxicity of a test substance administered to males and females at several concentrations in their daily diet prior to and during the breeding period and through gestation and lactation. Adverse effects on adult survival, oogenesis and/or spermatogenesis, reproductive indices, embryo or fetal development, and offspring growth and survival are measured. In the third protocol (primary vs secondary toxicity), the toxicity and lethality (LC50 value) of a test substance, in the form of the parent compound, administered via the diet in several concentrations to males and females (primary toxicity test) is compared with the toxicity and lethality of the same test substance fed at identical concentrations but contained in animal tissue (prey) contaminated by previous exposure to the same parent test substance (secondary toxicity test). Appropriate statistical procedures for assessing the data are presented for each protocol.

Substance (CAS Registry Number):
Sodium monofluoroacetate (62-74-8)
Aroclor 1254 (11097-69-1)

1988 - Pesticide Fact Sheet Number 174: Sodium Fluoracetate (Compound 1080).

Environmental Protection Agency, Washington, DC. Office of Pesticide Programs.

Order Number: NTIS/PB89-108724, 6p

The report contains up-to-date chemical information, including a summary of the Agency's regulatory position and rationale, on a specific pesticide or group of pesticides. A Fact Sheet is issued after one of the following actions has occurred; issuance/reissuance of a registration standard; issuance of each special review document; registration of a significantly changed use pattern; registration of a new chemical; or an immediate need for information to resolve controversial issues relating to a specific chemical or use pattern.

1988 - Health Assessment for Artel Chemical Company, Formerly Fike Chemical, Incorporated, City of Nitro, Putnam and Kanawha Counties, West Virginia, Region 3. CERCLIS No. WVD047989207.

Agency for Toxic Substances and Disease Registry, Atlanta, GA.

Order Number: NTIS/PB90-143918, 11p

The Artel Chemical Company site, formerly known as Fike Chemical Inc., manufactured specialty chemicals. There are many compounds on-site which are known to represent imminent and significant public health threats. Several compounds/contaminants of the most immediate concern are methyl mercaptan, bromine, sodium, ethyl and sodium fluoroacetate, and cyanide compounds. ATSDR has concluded that this site is of urgent public health concern because of the risk to human health resulting from the potential exposure to hazardous substances at concentrations that may result in acute health effects or death. Preliminary rept.

1985 - Compound 1080: Special Review Position Document 4.

Environmental Protection Agency, Washington, DC. Office of Pesticide Programs.

Order Number: NTIS/PB87-116471, 88p

The Position Document 4 (PD 4) concludes the Rebuttable Presumption Against Registration (RPAR) process for Sodium Monofluoroacetate, commonly called 'Compound 1080. Compound 1080 (1080) is currently used as a rodenticide on rangelands, croplands, and nonagricultural sites. Prior to 1972, 1080 was also used for predator control, principally for coyotes. In 1972, the predacidal uses of 1080 were cancelled. The RPAR document addresses only the rodenticidal uses of 1080.

Environmental surveys
Toxic substances
Compound 1080

1983 - Compound 1080, Sodium Monofluoroacetate: Position Document 2/3.

Environmental Protection Agency, Washington, DC. Office of Pesticide Programs.

Order Number: NTIS/PB87-182226, 116p

The Position Document addresses the risks and benefits of pesticide products containing the subject active ingredient. The Agency has determined that the use of products containing the subject active ingredient may meet or exceed a risk criterion described in 40 CFR Part 154. Potential hazards will be examined further to determine the nature and extent of the risk, and considering the benefits of the subject active ingredient, whether such risks cause unreasonable adverse effects on the environment. See also report dated Jul 85, PB87-116471.

Environmental surveys
Toxic substances
Compound 1080

1976 - Compound 1080 and 1081: Position Document 1

Environmental Protection Agency, Arlington, VA. Special Pesticide Review Div.

Order Number: NTIS/PB80-216823, 25p

The report is a preliminary risk assessment for Sodium Fluoroacetate and Fluoroacetamide. It gives a preliminary examination of its use, environmental residues, and health effects including toxicology data. Limited information is provided for exposure and extent of risk. Results of a literature search are provided.

Environmental surveys
Toxic substances
Acetic acid/fluoro

1980 - Monohaloacetic Acids.

Franklin Research Center, Silver Spring, MD.

Order Number: NTIS/PB92-206077, 100p

The monohaloacetic acids were reviewed, including information on occupational exposure, physical properties, toxicity, and structure/activity relationships. A detailed review and analysis was conducted of the biological effects of chloroacetic-acid (79-11-8), sodium-chloroacetate (3926-62-3), fluoroacetic-acid (144-49-0), sodium-fluoroacetate (62-74-8), iodoacetic-acid (64-69-7), sodium-iodoacetate (30-553-3), and bromoacetic-acid (7-908-3). Topics included: human effects; epidemiologic studies; animal toxicity; diagnosis; antidotes; absorption, distribution, metabolism, and excretion; biochemistry; mutagenicity; carcinogenicity; and teratogenicity. Accurate information on the number of workers potentially exposed to these compounds was not available. Sodium-fluoroacetate has been widely used as a mammalian pest control agent. Although these compounds have different modes of action, all of them inhibit various metabolic pathways. Based on the acute toxicity to rats, fluoroacetate was the most toxic. Sponsore [abstract truncated]

1978 - Identification and description of chemical deactivation detoxification methods for the safe disposal of selected pesticides.

Authors: Lande SS

Cent. Chem. Hazard Assess., Syracus Res. Corp., Syracuse, NY 13210

US NTIS PB Rep. PB-285,208: 188 p. 1978 (178 References)

... No acceptable chemical detoxification was found for the remaining pesticides: ronnel; dimethoate; dyfonate; DEF; EPTC; molinate; thiram; propanil; Diphenamid; chlorooxuron; simazine; cyanazine; Amitrole; praquat; PCNB; dinoseb; chloropicrin; chlorobenzilate; endrin; D-D; dibromochloropropane (DBCP); BHC; dicamba; sodium fluoroacetate (Compound 1080); creosote; and warfarin. (Author abstract by permission)

1950 - Treatment of Sodium Fluoroacetate Poisoning in Dogs and Rabbits.

Authors: Murtha EF, McNamara BP, Stabile DE, Wills JH

Chemical Corps, Army Chemical Center, MD.

Research rept. 23 Jun 49-3 Apr 50,

Order Number: NTIS/AD-A953 030/4, 13p

Sodium compounds



Toxicol Lett. 2004 Aug 1;151(3):399-406.
The traditional categories of fluoroacetate poisoning signs and symptoms belie substantial underlying similarities

Sherley M

RSPCA Australia, PO Box 265, Deakin West, Canberra 2600, Australia. msherley@rspca.org.au

Sodium monofluoroacetate (Compound 1080) has been widely used around the world as a vertebrate pest control agent. Following ingestion of 1080 there is a latent period, during which the compound is metabolised into a toxic form, before the onset of symptoms. The timing of this period varies significantly between species as does the median lethal dose. Traditionally different species have also been classified into groups depending on the primary organ system involved in 1080 toxicosis (cardiac, nervous, or mixed signs/symptoms). However, general acceptance of this method of classification has obscured the fact that several signs of fluoroacetate poisoning are common to most vertebrate species. This paper reviews five decades of literature on the signs/symptoms of fluoroacetate poisoning in vertebrates and concludes that there is little justification for the division of animals poisoned by fluoroacetate into symptomatic groups.

Publication Types:
• Review
• Review, Tutorial

PMID: 15261984 [PubMed - indexed for MEDLINE]


J Toxicol Sci. 2004 May;29(2):155-66.
Neurotoxic effects of alpha-fluoro-beta-alanine (FBAL) and fluoroacetic acid (FA) on dogs.

Yamashita K, Yada H, Ariyoshi T.

Pharmacokinetics Research Laboratory, Taiho Pharmaceutical Co., Ltd., 224-2 Ebisuno, Hiraishi, Kawauchi-cho, Tokushima 771-0194, Japan.

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.

PMID: 15206584 [PubMed - indexed for MEDLINE]


Biochim Biophys Acta. 2004 Apr 8;1698(1):27-36.
Reactivity of asparagine residue at the active site of the D105N mutant of fluoroacetate dehalogenase from Moraxella sp. B.

Ichiyama S, Kurihara T, Kogure Y, Tsunasawa S, Kawasaki H, Esaki N.

Laboratory of Microbial Biochemistry, Institute for Chemical Research, Kyoto University, Uji, Kyoto 611-0011, Japan.

Fluoroacetate dehalogenase from Moraxella sp. B (FAc-DEX) catalyzes cleavage of the carbon-fluorine bond of fluoroacetate, whose dissociation energy is among the highest found in natural products. Asp105 functions as the catalytic nucleophile that attacks the alpha-carbon atom of the substrate to displace the fluorine atom. In spite of the essential role of Asp105, we found that site-directed mutagenesis to replace Asp105 by Asn does not result in total inactivation of the enzyme. The activity of the mutant enzyme increased in a time- and temperature-dependent manner. We analyzed the enzyme by ion-spray mass spectrometry and found that the reactivation was caused by the hydrolytic deamidation of Asn105 to generate the wild-type enzyme. Unlike Asn10 of the l-2-haloacid dehalogenase (L-DEX YL) D10N mutant, Asn105 of the fluoroacetate dehalogenase D105N mutant did not function as a nucleophile to catalyze the dehalogenation.

PMID: 15063312 [PubMed - indexed for MEDLINE]


J Am Chem Soc. 2003 Jan 15;125(2):379-87.
Assay for the enantiomeric analysis of [2H1]-fluoroacetic acid: insight into the stereochemical course of fluorination during fluorometabolite biosynthesis in streptomyces cattleya.

O'Hagan D, Goss RJ, Meddour A, Courtieu J.

School of Chemistry, University of St Andrews, Centre of Biomolecular Sciences, North Haugh, United Kingdom, KY15 9EA.

A sensitive method for the configurational analysis of (R)- and (S)-[2H1]-fluoroacetate has been developed using 2H[1H]-NMR in a chiral liquid crystalline solvent. 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. In particular, feeding experiments to S. cattleya with isotopically labeled (1R, 2R)- and (1S, 2R)-[1-2H1]-glycerol 3d and 3e and [2,3-2H(4)]-succinate 4a gave rise to samples of enantiomerically enriched [2-2H1]-fluoroacetates 1a. The predominant enantiomer resulting from each experiment suggests that the stereochemical course of biological fluorination takes place with an overall retention of configuration between a glycolytic intermediate and fluoroacetate 1. Consequently, this outcome suggests that the stereochemical course of the recently identified fluorinase enzyme which mediates a reaction between fluoride ion and S-adenosyl-l-methionine (SAM), occurs with an inversion of configuration.

PMID: 12517149 [PubMed - indexed for MEDLINE]


Chem Commun (Camb) 2002 Jul 7;(13):1428-9

A screening system for enantioselective enzymes based on differential cell growth.

Reetz MT, Ruggeberg CJ.

Max-Planck-Institut fur Kohlenforschung, D-45470 Mulheim/Ruhr, Germany. reetz@mpi-muelheim.mpg.de

The esterase-catalyzed enantioselective hydrolysis of the fluoroacetate of pantolactone leads to fluoroacetic acid, a toxic compound which inhibits the growth of esterase-producing yeast; this forms the basis of an ee-assay.

PMID: 12125587 [PubMed - indexed for MEDLINE]


Vet Hum Toxicol 2002 Apr;44(2):93-5

Intoxication with sodium monofluoroacetate (compound 1080).

Robinson RF, Griffith JR, Wolowich WR, Nahata MC.

Pediatric Pharmacotherapy/NIH Clinical Research K30 Program, College of Pharmacy, The Ohio State University, Childrens Research Institute, The Central Ohio Poison Control Center, Columbus 43210, USA.

The highly toxic sodium monofluoroacetate (SMFA) was banned as a rodenticide in the U.S. in 1972. We report the first case of intentional ingestion in this country in over 15y. A 47-y-old male was brought to the emergency room status post tonic clonic seizure. At 34 h post ingestion, he responded ony to noxious stimuli and at 48 h, he was unresponsive to painful stimuli, was intubated and placed on a ventilator. Over the following 3 d, he was became minimally responsive to external stimuli with bouts of agitation and hypertension. Two days later he was discharged with no evidence of neurologic sequelae. We report this patient to increase awareness of SMFA toxicity, and its ability to cause anion gap metabolic acidosis.

PMID: 11931513 [PubMed - indexed for MEDLINE]


Nucl Med Biol 2002 Apr;29(3):303-6

In vitro uptake of [1-14C]Octanoate in brain slices of rats: basic studies for assessing [1-11C]Octanoate as a PET tracer of glial functions.

Kuge Y, Hikosaka K, Seki K, Ohkura K, Nishijima K, Tsukamoto E, Tamaki N.

Department of Tracer Kinetics, Graduate School of Medicine, Hokkaido University, Kita 15 Nishi 7, Kita-ku, 060-8638, Sapporo, Japan. kuge@med.hokudai.ac.jp

To clarify the contribution of glial cells to octanoate uptake into the brain, we determined the effects of fluoroacetate, a selective inhibitor of glial metabolism, on in vitro brain uptake of [1-14C]octanoate, using rat brain slices. The [1-14C]octanoate uptake significantly decreased, depending on the concentration of fluoroacetate (p = 0.001). The [1-14C]octanoate uptakes at 5 mM (0.23 +/- 0.05% uptake/mg slice) and 25 mM fluoroacetate (0.12 +/- 0.01% uptake/mg slice) were significantly lower than that at control (0.29 +/- 0.02% uptake/mg slice, p < 0.05 and p < 0.001, respectively). The results demonstrate the contribution of glial cells to octanoate uptake into the brain. The potential of [1-11C]octanoate as a PET tracer for studying glial functions is suggested.

PMID: 11929699 [PubMed - indexed for MEDLINE]


Toxicology. 2002 Dec 27;181-182:523-30.
Sodium monofluoroacetate (1080) risk assessment and risk communication.

Eason C.

CENTOX (Centre for Environmental Toxicology) Landcare Research, P.O. Box 69, Lincoln 8152, New Zealand. easonc@landcare.cri.nz

Sodium monofluoroacetate (1080) is a vertebrate pesticide widely used for possum control in New Zealand. Fluoroacetate is also a toxic component of poisonous plants found in Australia, South Africa, South America, and India. Because of its importance and effectiveness in pest control and the highly toxic nature of this compound, its acute sub-lethal and target organ toxicity have been extensively studied. In relation to its use as a pesticide its environmental fate, persistence, non-target impacts and general toxicology have been and continue to be extensively studied. Toxic baits must be prepared and used with extreme care, otherwise humans, livestock, and non-target wildlife will be put at risk. The high risk of secondary poisoning of dogs is a cause for concern. 1080 acts by interfering with cellular energy production. Possums die from heart failure, usually within 6-18 h of eating baits. Long-term exposure to sub-lethal doses can have harmful effects and strict safety precautions are enforced to protect contractors and workers in the bait manufacturing industry. Considerable care is taken when using 1080 to ensure that the risks of using it are outweighed by the ecological benefits achieved from its use. When its use is controversial, risk communicators must take care not to trivialise the toxicity of the compound. The benefits of 1080 use in conservation, pest control, and disease control should be weighed up alongside the risks of using 1080 and other techniques for pest control.

Publication Types:
• Review
• Review, Tutorial

PMID: 12505362 [PubMed - indexed for MEDLINE]


Wei Sheng Yan Jiu. 2002 Aug;31(4):316-8.

[Advances in the detection method of several forbidden rodenticides]

[Article in Chinese]

Xie W, Chen Z, Li X.

National Poison Control Center, Chinese Academy of Preventive Medicine, Beijing 100050, China.

The progress of detection method of four forbidden rodenticides, including fluoroacetamide, sodium fluoroacetate, gliftor and tetramine is reviewed in this paper. The technique of sample preparation and gas chromatography are emphasized.

Publication Types:
• Review
• Review, Tutorial

PMID: 12600049 [PubMed - indexed for MEDLINE]


Eur J Neurosci 2000 Mar;12(3):856-62

Metabolic coupling between glia and neurons is necessary for maintaining respiratory activity in transverse medullary slices of neonatal mouse.

Hulsmann S, Oku Y, Zhang W, Richter DW.

Zentrum Physiologie und Pathophysiologie, Abt. Neuro- und Sinnesphysiologie, Georg-August-Universitat, Humboldtallee 23, 37073 Gottingen, Germany. swen@neuro-physiol.med.uni-goettingen.de

The respiratory rhythm is generated and regulated by a neuronal network within the lower brainstem. While the neuronal mechanisms of rhythm generation have been extensively investigated, the contribution of glial cells remains to be determined. Here we report the effect of specific blockade of the glial Krebs cycle and glutamine synthetase on the neuronal activity of the respiratory network. Application of 5 mM fluoroacetate, which selectively blocks the glial Krebs cycle, suppressed rhythmic respiratory burst activity. Substitution of either the Krebs cycle substrate isocitrate (3 mM) or glutamine (3 mM) restored rhythmic network activity. Blockade of glutamine synthetase by methionine sulfoximine (0.5 mM) suppressed rhythmic burst activity as well. Resubstitution of glutamine (3 mM) was able to restore rhythmic activity in the presence of methionine sulfoximine. This data demonstrates that the glutamate-glutamine cycle in astrocytes and their supply of glutamine to neuronal glutamatergic terminals is essential for the rhythm generation in the respiratory centre.

PMID: 10762315 [PubMed - indexed for MEDLINE]

From Dart Specdial at Toxnet

Proceedings of the New Zealand Society of Animal Production 1999;59:250-3

Toxicity effects of 1080 on pregnant ewes.

O'Connor CE, Milne LM, Arthur DG, Ruscoe WA, Wickstrom M

Centre for Environmental Toxicology, Landcare Research, Lincoln, New Zealand.

There are no data on the potential for 1080 used for pest control to cause delayed deaths or impaired productivity in livestock following multiple, sub-lethal doses. Recent losses of late-gestation ewes exposed to weathered 1080 baits has also led to speculation that pregnant ewes may be unusually sensitive to the toxin. To address these data gaps, groups of 20 Perendale ewes, non-pregnant or pregnant with twins, were administered either a single (0.25 mg/kg) or multiple oral doses (0.05 mg/kg over 3 consecutive days) of a 1080 cereal pellet. The highest mortality occurred in the single dose groups (pregnant 45%, non-pregnant 21%) compared to the multiple dose groups (pregnant 35%, non-pregnant 0%). There was no mortality in the control group of pregnant ewes. Log-linear modelling showed highly significant treatment effects (P = 0.0003) and differences (P = 0.045) in acute mortality rates between pregnant (40%) and non-pregnant ewes (10%), which was linked to increased bioavailablity. There were no differences in the incidence of metabolic diseases, lambing percentages, lamb survival, or growth rates between dosed and undosed pregnant ewes. This study demonstrated that extra care should be taken to avoid exposure of pregnant ewes to even small bait fragments, but also provides further evidence that there are no long-term health effects in animals that survive accidental 1080 poisoning.


Hum Exp Toxicol 1999 Jun;18(6):351-3

Hemodynamic abnormalities in sodium monofluoroacetate intoxication.

Chi CH, Lin TK, Chen KW.

Department of Emergency Medicine, National Cheng-Kung University Medical College and Hospital, Tainan City, Taiwan.

Hypotension is one of the most important predictors of mortality in sodium monofluoroacetate (SMFA) intoxication. This paper reports the hemodynamic response in one fatal and another survival case of SMFA intoxication. Despite correction of hypovolemia and with inotropic support, the patients remained in shock. Hemodynamic observations have provided evidence that shock after SMFA intoxication is due to diminished systemic vascular resistance and increased cardiac output. This is the first report in which such an invasive hemodynamic investigation has been recorded in a clinical case of SMFA intoxication.

PMID: 10413241 [PubMed - indexed for MEDLINE]


No Abstract available

Bull Environ Contam Toxicol 1999 Jan;62(1):34-9

Degradation of sodium monofluoroacetate (1080) and fluorocitrate in water.

Booth LH, Ogilvie SC, Wright GR, Eason CT.

Landcare Research, Post Office Box 69, Lincoln, New Zealand.

PMID: 9870987 [PubMed - indexed for MEDLINE]

From Dart Specdial at Toxnet

Toxicologist 1998 Mar;42(1-S):258-9

Assessment of the developmental toxicity of sodium monofluoroacetate (1080) in rats.

Turck PA, Eason CT, Wickstrom M

MPI Research, Mattawan, MI.

1080 has been used in New Zealand to control vertebrate pests since 1954, and although a large historical database exists, little is known about the developmental toxicity of this pesticide. This investigation was intended to evaluate the developmental toxicity and teratogenic potential of 1080 in Sprague-Dawley rats following oral intubation. A pilot study was performed to help select doses for the subsequent study and consisted of groups of 5 time-mated females. Animals received 1080 at concentrations ranging from 0.1 to 1.0 mg/kg/day from Days 6 to 17 of gestation. A 60% mortality rate and reductions in maternal body weight and body weight gain as well as decreased litter size and increased resorptions were observed at 1.0 mg/kg/day. Consequently, the doses selected for the main study were 0.1, 0.33 and 0.75 mg/kg/day. Groups of 26 time-mated females received 1080 from Days 6 to 17 of gestation. On Day 20 of gestation, litters were delivered via laparohysterectomy. The results of this study have not been fully evaluated, but visceral and skeletal evaluation results will be presented. Significant reductions in maternal body weight, body weight gain and food consumption were noted at 0.75 mg/kg/day. No changes in litter size or resorptions were observed, but fetal body weight was significantly reduced at 0.75 mg/kg/day. No external fetal abnormalities were noted. Available data indicate that 1080 is maternally toxic at 0.75 mg/kg/day and higher. Embryolethality was noted at 1.0 mg/kg/day, but not at 0.75 mg/kg/day. At this stage, there is no evidence of developmental toxicity. Reductions in fetal body weight at 0.75 mg/kg/day are probably linked to maternal toxicity rather than a direct effect on the fetus.

From Science Direct

Toxicology Letters; Volume 95, Supplement 1 , July 1998, Page 105

The subcellular distribution of defluorination activity in three mammalian species

L. Tu (1), C. Rix (2), P. F. A. Wright (1) and J. T. Ahokas (1)

1 Key Centre for Applied and Nutritional Toxicology Melbourne VIC 3000 Australia
2 Applied Chemistry, RMIT-University Melbourne VIC 3000 Australia

Fluoroacetate is highly toxic to a wide range of animals, including non-target species. The species difference in sensitivity to fluoroacetate remains without an explanation. In mammals, detoxication of fluoroacetate by defluorination occurs mainly in the liver by fluoroacetate-specific defluorinase. This enzyme is thought to be a unique glutathione-S-transferase, but the mechanism of this glutathione dependent reaction is still unclear. To understand the species differences in fluoroacetate sensitivity, subcellular fractionation of liver from Wistar rats, Bal b/c mice and brushtail possums (Trichosurus vulpecula) was performed. Defluorination was measured by fluoride ion determination in vitro based on fluoride release after incubation, using sodium fluoroacetate as the substrate. The results showed:
1) Defluorination activity based on protein content was the highest in the cytosolic fraction in all species. The mitochondrial and microsomal fractions both had minimal activity.
2) The subcellular distribution of defluorination activity in the liver of male rats showed the nuclear, mitochondria, microsomes and cytosol presented 33.2%, 0.6%, 1.3% and 50.8%, respectively, of the defluorination activity in the homogenate.
3) The comparison between male and female of rats and mice suggested that there was increasing defluorination activity, in females. However, only the cytosolic fraction of female rats had significantly higher activity (203.66 ng of F/mg protein/hr) than male rats (161.80 ng of F/mg protein/hr) (P < 0.05).
4) Comparison of defluorination activity in the three species showed that rats and possums had a relatively lower activity in cytosol, but higher activity in mitochondria and microsomes compared with mice (P < 0.01). The rank order of defluorination activity in the mitochondrial fraction in the three species is possum> rat> mouse (P < 0.01).
This study suggested that the defluorination of fluoroacetate is mainly localised in cytosolic fraction of the liver. Female animals presented a higher defluorination activity tendency. The role of mitochondria in defluorination of fluoroacetate requires further investigation.


No Abstract available

Bull Environ Contam Toxicol 1998 May;60(5):745-9

Uptake and persistence of sodium monofluoroacetate (1080) in plants.

Ogilvie SC, Booth LH, Eason CT.

Manaaki Whenua, Lincoln, New Zealand.

PMID: 9595190 [PubMed - indexed for MEDLINE]


J Toxicol Clin Toxicol 1996;34(6):707-12

Clinical presentation and prognostic factors in sodium monofluoroacetate intoxication.

Chi CH, Chen KW, Chan SH, Wu MH, Huang JJ.

Department of Emergency Medicine, National Cheng Kung University Hospital, Tainan, Taiwan, ROC.

BACKGROUND: The diagnosis of sodium monofluoroacetate intoxication in humans is usually based on a history of ingestion and clinical findings. Although several previous reports have described the clinical course and outcome of patients who ingested this drug, prognostic indicators of short-term survival are not available.
METHODS: A retrospective study of 38 consecutive cases of sodium monofluoroacetate poisoning at the National Cheng Kung. University Hospital, 1988-1993, to analyze the clinical findings and to predict mortality.
RESULTS: Seven of 38 patients (18%) died. The most common symptom was nausea or vomiting (74%). The most frequent ECG finding was nonspecific ST-T and T wave abnormalities (72%). Hypocalcemia (42%) and hypokalemia (65%) were the common electrolyte abnormalities. The clinical and laboratory characteristics were compared for the survival and mortality groups. Significant differences in hypotension, respiratory rate, pulse rate, creatinine, potassium, elevated alanine aminotransferase, pH, PCO2, APACHE II score, and subjective respiratory distress were noted. Discriminant analysis identified hypotension, increased serum creatinine, and decreased pH as the most important predictors of mortality, with sensitivity of 86% and specificity of 96%.
CONCLUSIONS: Hypotension and the early onset of metabolic acidosis and increased serum creatinine are associated with poor short-term survival. These prognostic variables can be useful in the care of patients with suspected sodium monofluoroacetate intoxication. It is suggested that all such patients should be observed intensively for at least 48 h.

PMID: 8941201 [PubMed - indexed for MEDLINE]


No Abstract available

Bull Environ Contam Toxicol 1995 Jul;55(1):162-9

Sodium monofluoroacetate (1080) leaching through soils.

Parfitt RL, Eason CT, Hoff H, Heng LK.

Manaaki Whenua-Landcare Research, Palmerston North, New Zealand.

PMID: 7663087 [PubMed - indexed for MEDLINE]

From Dart Special at Toxnet

Chemically Induced Birth Defects 1993;2:675-721


Schardein JL

International Research and Development Corporation, Mattawan, MI.

Medical Subject Headings (MeSH):
*Abnormalities, Drug-Induced
2,4,5-Trichlorophenoxyacetic Acid/TOXICITY

Substance (CAS Registry Number): [Too many to list]

Sodium fluoroacetate (62-74-8)

[Note: the following organofluorines were included]
Diflubenzuron (35367-38-5)
Ethalfluralin (55283-68-6)
Flusilazole (85509-19-9)
Gliftor (8065-71-2) - [Synonym: 1-Chloro-3-fluoro-2-propanol mixt. with 1,3-difluoro-2-propanol]
N-Methyl-N- 1-naphthyl fluoroacetamide [Nissol] (5903-13-9)
Sarin [Synonym: (+-)-Isopropyl methylphosphonofluoridate] (107-44-8)
Sodium fluoroacetate (62-74-8)
Sodium hexafluorosilicate [also known as Sodium fluorosilicate] (16893-85-9)
Soman [Synonym: 1,2,2-Trimethylpropyl methylphosphonofluoridate] (96-64-0)
Sulfuryl fluoride (2699-79-8)
Trifluralin (1582-09-8)


Am Ind Hyg Assoc J 1992 May;53(5):298-302

The development of cleanup criteria for an acutely toxic pesticide at a contaminated industrial facility.

LaGoy PK, Bohrer RL, Halvorsen FH.

OHM Remediation Services Corp., Walnut Creek, CA 94596.

Sodium fluoroacetate, a restricted-use rodenticide, was improperly applied to kill rats in a South American steel mill. As a result of this application, several workers were seriously injured. During plant decontamination, cleanup levels were developed to ensure that any residual material remaining at the plant did not pose a health risk. Cleanup levels were developed to prevent significant exposure of workers, who could inhale contaminated dust, contact dust, or soil dust in outdoor areas or on plant floors and who could contact contaminated surfaces. On the basis of a health risk analysis, the following cleanup levels for sodium fluoroacetate were developed--air cleanup levels, 0.05 mg/m3; soil/dust cleanup levels, 100 mg/kg; and wipe sample cleanup levels, 0.2 mg/100 cm2. These risk-based cleanup levels were ultimately used to assist the regulatory agencies in reaching a decision to reopen the plant.

PMID: 1609740 [PubMed - indexed for MEDLINE]


Ann N Y Acad Sci 1992 Jun 16;653:356-66

Mongoose rabies in the Caribbean.

Everard CO, Everard JD.

Leptospira Laboratory, St. Michael, Barbados.

Mongooses (Herpestes auropunctatus) have been introduced into most of the larger Caribbean islands, some notable exceptions being Dominica, Tobago, and Montserrat. Rabies in Caribbean mongooses is present in Puerto Rico, Cuba, the Dominican Republic (and presumably Haiti), and Grenada. Bat rabies is known on Cuba, Grenada, and Trinidad, although mongooses found on Trinidad are free of the disease. None of the other islands is known to have rabies, although it could be present in sequestered bat populations. All reported case numbers of mongoose rabies in the Caribbean are underestimates, and available information is at best incomplete and at times fragmentary. Nevertheless, data are presented from the four affected islands. Mongoose reduction campaigns have been undertaken on Cuba and Grenada. In Cuba strychnine sulfate inoculated into labeled eggs is used, whereas in Grenada sodium fluoroacetate (1080) has been used in boiled cowhide baits. Mongoose poisoning is unsatisfactory and ineffective in the long-term. Because many mongooses naturally exposed to rabies virus develop serum neutralizing antibodies and are considered to be immunized, possibly for life, vaccination in the wild has been under consideration since the mid-1970s. Early attempts to produce a pill coated with ERA vaccine for enteric absorption in mongooses were not very successful, but new modified vaccines and recombinant techniques hold considerable promise.

Publication Types: Review; Review, Tutorial

PMID: 1626884 [PubMed - indexed for MEDLINE]


Brain Res 1990 Dec 10;535(2):205-13

Glucose-supported oxidative metabolism and evoked potentials are sensitive to fluoroacetate, an inhibitor of glial tricarboxylic acid cycle in the olfactory cortex slice.

Saito T.

Department of Physiology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan.

Optical absorbance change was measured by reflectance spectrophotometry in the olfactory cortex slice prepared from the rat brain. Optical absorbance of the piriform area of the slice was increased by perifusion with an anoxic (N2-gassed) solution. Components of the absorbance spectrum recorded from the slice in anoxia corresponded to that of cytochromes (cyt) aa3 and c + c1, but did not to that of cyt c. Reduction of cytochromes in anoxia coincided with decrease in the amplitude of the presynaptic potential and a slower negative wave (N-wave). The reduced state of cytochromes switched to an oxidized state when a well-oxygenated solution was reintroduced. An almost complete recovery of redox state coincided with full recovery of the evoked potential. A metabolic inhibitor, 2-deoxy-D-glucose (2DG) (10 mM) or iodoacetic acid (IAA) (3 mM) caused little or slight oxidation of cytochromes, but significantly decreased the amplitude of evoked potentials. Marked oxidation of cytochromes was observed only by perifusion with a solution containing 2 DG (10 mM) and IAA (3 mM). The rate of oxygen uptake was significantly lowered by these metabolic inhibitors. When the slice was perifused with a solution containing fluoroacetate (1 or 10 mM), a selective inhibitor of glial metabolism, cytochromes shifted to oxidized levels. The amplitude of evoked potentials tended to decline by a low dose (1 mM), and significantly decreased by a high dose (10 mM) of fluoroacetate. Oxygen consumption of the slice was dose-relatedly lowered by fluoroacetate.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 2073603 [PubMed - indexed for MEDLINE]


Acta Neuropathol (Berl) 1990;81(1):66-73

Experimental neurotoxicity of 5-fluorouracil and its derivatives is due to poisoning by the monofluorinated organic metabolites, monofluoroacetic acid and alpha-fluoro-beta-alanine.

Okeda R, Shibutani M, Matsuo T, Kuroiwa T, Shimokawa R, Tajima T.

Department of Neuropathology, Tokyo Medical & Dental University, Japan.

Two metabolites of 5-fluorouracil (FU), monofluoroacetic acid (FA) and alpha-fluoro-beta-alanine (FBAL), were continuously administered into the left ventricle of the brain in cats for up to 1 month to investigate the mechanism of neurotoxicity of FU and its derivatives. The cumulative doses of FU and FBAL over a 1-month period were 1.5-45 mg (20 cats) and 0.2-4.8 mg (21 cats), respectively. As controls for each experimental group, acetic acid (AA) and beta-alanine (BAL) were administered. In terms of survival time in relation to the cumulative dose and molecular weight, FBAL was more toxic than FA. Neuropathologically, two types of change, vacuoles and necrosis/softening-like change, were found. The vacuoles were 20-50 microns in diameter, and distributed mainly in the cerebellar nuclei, white matter and the tectum and tegmentum of the brain stem in both experimental groups. Electron microscopically, these vacuoles were due to splitting of the myelin intraperiod line or separation between the axon and the innermost layer of myelin. Necrosis/softening-like change occurred preferentially in the FBAL group and was located symmetrically in the superior and inferior colliculi, oculomotor nuclei and thalamus. Both types of neuropathological change, especially those in the FBAL group, were similar to those found in cats orally administered with FU and its derivatives.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 2128162 [PubMed - indexed for MEDLINE]


No Abstract available

Biochim Biophys Acta 1989;1000:254-69

The toxicity of fluoroacetate and the tricarboxylic acid cycle. 1949.

Liebecq C, Peters RA.

Publication Types:

  • Biography
  • Classical Article
  • Historical Article

Personal Name as Subject:

  • Liebecq C
  • Peters RA

PMID: 2673373 [PubMed - indexed for MEDLINE]


Braz J Med Biol Res 1989;22(8):975-7

Is monofluoracetic acid the active neurotoxic principle in Palicourea marcgravii (St. Hill) leaves?

Eckschmidt M, Brizolla M, Tarraga DP, Palermo-Neto J.

Departamento de Patologia, Faculdade de Medicina Veterinaria e Zootecnia, Universidade de Sao Paulo, Pirassununga, Brasil.

Acute intoxication of rats with the crude extract of Palicourea marcgravii (PM) and with monofluoracetic acid (MFA) solutions was compared since it has been reported that PM leaves contain monofluoracetates (455 micrograms/g air-dried material). The neurotoxic signs produced by oral administration of PM and MFA were similar and included tonic-clonic seizures. The dose-response curves constructed for the convulsant effects of PM and MFA were parallel and the CD50s were 630 mg/kg (508-781) and 0.90 mg/kg (0.76-1.06), respectively. These data suggest that the neurotoxic signs produced by PM are the consequence of MFA present in the plant leaves.

PMID: 2633850 [PubMed - indexed for MEDLINE]

From Science Direct

Comparative Biochemistry and Physiology Part C: Comparative Pharmacology; Volume 91, Issue 2 , 1988, Pages 343-347

The effect of sodium monofluoroacetate on plasma testosterone concentration in Tiliqua rugosa (gray)

L. E. Twigg*, D. R. King† and A. J. Bradley‡

* School of Environmental and Life Sciences, Murdoch University, Murdoch, Western Australia, 6150
† Agriculture Protection Board, Bougainvillea Avenue, Forrestfield, Western Australia, 6058
‡ Department of Zoology, University of Western Australia, Nedlands, W.A. 6009, Australia
Received 18 August 1987.  Available online 17 May 2004.

1. 1. Administration of multiple or single doses of sodium fluoroacetate (1080) to male Tiliqua rugosa caused a decrease in plasma testosterone concentration.
2. 2. A single dose of 100 or 250 mg 1080 kg-1 body weight decreased plasma testosterone by 52%. However, 25 mg kg-1 had little apparent effect on testosterone levels. When lizards were given the multiple dose equivalent of these doses over 12 days at 3 day intervals, the effect was much less dramatic with plasma testosterone concentration steadily declining over 15 days for the two higher doses.
3. 3. There was a suggestion of degeneration of seminiferous tubules in some individuals.


J Assoc Off Anal Chem 1988 May-Jun;71(3):579-81

Tissue fluoroacetate residues in prairie dogs dosed with low-level sodium monofluoroacetate.

Hugghins EJ, Casper HH, Ward CD.

South Dakota State University, Biology Department, Brookings 57007.

A total of 83 black-tailed prairie dogs (Cynomys ludovicianus) from South Dakota were subjected to low-level treatment with sodium monofluoroacetate (Compound 1080) in the laboratory (0.01-0.30 mg 1080/kg). The acute oral median lethal dose (LD50) of 1080 administered by oral gavage was established at 0.173 mg/kg. To assay fluoroacetate residues, 8 kinds of tissue from each of 10 prairie dogs dead of low-level 1080 poisoning were analyzed by capillary gas chromatography-mass spectrometry. Of the total of 79 tissues analyzed, 73 contained less than 100 ppb fluoroacetate, and 67 contained less than 50 ppb fluoroacetate. To test the effect of secondary poisoning on non-target species, 8 European ferrets (Mustela furo) were fed ground whole carcasses of prairie dogs dead of low-level 1080 poisoning, with no observable ill effects on the ferrets.

PMID: 3391967 [PubMed - indexed for MEDLINE]


No Abstract available

Bull Environ Contam Toxicol 1988 May;40(5):707-10

Sodium monofluoroacetate (1080): a study of residues in arctic fox muscle tissue.

Tietjen H, Deines F, Stephensen W.

Denver Wildlife Research Center, U.S. Department of Agriculture, Colorado 80225.

PMID: 3382787 [PubMed - indexed for MEDLINE]


Bull Environ Contam Toxicol 1987 Jun;38(6):934-6

No Abstract available

Acute toxicity of sodium monofluoroacetate to the striped skunk.

Eastland WG, Beasom SL.

PMID: 3580616 [PubMed - indexed for MEDLINE]


Arch Environ Contam Toxicol 1987 May;16(3):357-66

No Abstract available

Primary and secondary toxicity of warfarin, sodium monofluoroacetate, and methyl parathion in mink.

Aulerich RJ, Ringer RK, Safronoff J.

PMID: 3592762 [PubMed - indexed for MEDLINE]


Brain Res 1987 Apr 28;410(1):116-20

Increase in the stimulation-induced overflow of glutamate by fluoroacetate, a selective inhibitor of the glial tricarboxylic cycle.

Szerb JC, Issekutz B.

Fluoroacetate is known to be taken up selectively by glia, where after forming fluorocitrate, it inhibits the tricarboxylic acid cycle. Since uptake into glia has a major role in the inactivation of synaptically released glutamate, the effect of fluoroacetate on the overflow of glutamate evoked by electrical field stimulation in slices of rat hippocampus was investigated. In agreement with previous reports, 1 mM fluoroacetate reduced the release and content of glutamine, but increased only slightly the overflow of glutamate induced by stimulation. If, however, 0.5 mM glutamine was added to the superfusion fluid, fluoroacetate nearly tripled the overflow of glutamate evoked by electrical field stimulation. The large glutamate overflow due to field stimulation in the presence of fluoroacetate was fully Ca2+ -dependent. Results confirm the major role of glia in the inactivation of glutamate. The absence of such an uptake may contribute to the in vivo convulsive effect of fluoroacetate.

PMID: 2884018 [PubMed - indexed for MEDLINE]

From Toxline at Toxnet

Vet. Hum. Toxicol.; VOL 28 ISS Apr 1986, P154

Inebriation with pyridoxine and fluoroacetate: case report

Ramirez M

Centro Toxicologico Regional Ctr. Occidental, Apartado Postal 658, Barquisimeto 3001, Lara, Venezuela

IPA COPYRIGHT: ASHP A case report of a 29-yr-old male, demonstrating the antidotal properties of ethyl alcohol in sodium fluoroacetate (Exterminio) poisoning, is described. The man had ingested fluoroacetate with alcohol and was brought to the hospital. Administration of pyridoxine antagonized the alcohol effects, and a fluoroacetate induced grand mal seizure occurred.


J Assoc Off Anal Chem 1986 May-Jun;69(3):441-2

Fluoroacetate residues in ground squirrel and coyote tissues due to primary or secondary 1080 poisoning.

Casper HH, Mount ME, Marsh RE, Schmidt RH.

Fluoroacetate residues in various tissues of 1080-poisoned ground squirrels and coyotes are listed. The tissues (excluding the stomach) of squirrels poisoned with an average of 0.8 mg 1080/kg (low dose) contained from 182 to 1309 ppb fluoroacetate. In squirrels poisoned with an average of 4.8 mg 1080/kg (high dose), the tissue residues ranged from 535 to 9754 ppb fluoroacetate. Tissues from coyotes which died after consuming 1080-poisoned ground squirrels were also analyzed for fluoroacetate residues. Residues in these coyote kidneys and livers ranged from less than 10 ppb to 95 ppb fluoroacetate. The residue findings in this research indicate that a diagnostic assay for 1080 in tissues must be reliable at 10 ppb (or less) fluoroacetate.

PMID: 3722090 [PubMed - indexed for MEDLINE]


Aust J Biol Sci 1986;39(1):1-15

Metabolism of fluoroacetate in the skink (Tiliqua rugosa) and the rat (Rattus norvegicus).

Twigg LE, Mead RJ, King DR.

Administration of 100 mg sodium fluoroacetate (compound 1080) per kilogram body weight to T. rugosa resulted in a 3.4-fold increase in plasma citrate levels 48 h after dosing while administration of 3 mg sodium fluoroacetate per kilogram body weight to R. norvegicus produced a fivefold increase in plasma citrate levels within 4 h. Administration of 300 mg sodium fluoroacetate per kilogram body weight reduced the oxygen consumption of the skink by between 2.5 and 11% while in the rat, 2 mg sodium fluoroacetate per kilogram body weight reduced oxygen consumption by between 28 and 57%. Aconitate hydratase activity in extracts of liver acetone powders from T. rugosa was less inhibited by (-)erythrofluorocitrate (Ki: 0.065 mM) than that in extracts derived from R. norvegicus (Ki: 0.026 mM). The rate of defluorination of fluoroacetate in erythrocytes and in extracts of liver acetone powders of T. rugosa was 8- and 4.5-fold greater, respectively, than that found in similar preparations from R. norvegicus. A rapid rate of defluorination together with a low reliance on aerobic respiration favoured detoxification of fluoroacetate in T. rugosa rather than its conversion into fluorocitrate. Though defluorination in this species helped to minimize the immediate effects of fluoroacetate on aerobic respiration, it resulted in rapid depletion of liver glutathione levels.

PMID: 3778356 [PubMed - indexed for MEDLINE]

• Skink - alert agile lizard with reduced limbs and an elongated body covered with shiny scales; more dependent on moisture than most lizards; found in tropical regions worldwide

From Dart Special at Toxnet

DISS ABSTR INT B 46:1497,1986



Taxonomic Name:
Test Object: MAMMAL, MINK

Name of Agent (CAS RN):
O-CRESOL ( 95-48-7 )
THIRAM ( 137-26-8 )
AROCLOR 1254 ( 11097-69-1 )

Route of Administration: PER ORAL DIET


No Abstract available

Vet Hum Toxicol 1985 Feb;27(1):20-1

Toxic ducks--1080 residues in game birds. An exercise in applied toxicology.

Temple WA, Edwards IR.

PMID: 3976163 [PubMed - indexed for MEDLINE]


J Assoc Off Anal Chem 1984 May-Jun;67(3):549-53

Gas chromatographic analysis of coyote and magpie tissues for residues of compound 1080 (sodium fluoroacetate).

Okuno I, Connolly GE, Savarie PJ, Breidenstein CP.

Tissues of coyotes and magpies administered known dosages of 1080 were analyzed for residues by an analytical method specifying gas chromatography and electron capture detection. The repeatability of the method was determined for the replicate analyses of coyote muscle tissue samples aged under different storage conditions. The average coefficient of variation (CV) was 6% for quadruplicate determinations of 1080 in fresh tissues, 12-14% for samples stored at - 10 degrees C for 30-60 days, and 24% for samples aged for 7 days at ambient temperatures. The larger CV value obtained for stored samples is attributed more to greater sample variability than to less precision of the analytical method. Residues of 1080 appear to be relatively stable in tissues; there was essentially no change in the concentration of 1080 in samples stored up to 28 days at ambient temperature. Residue levels in the muscle, heart, kidney, and intestine were comparable, slightly lower in the liver, and much higher in the stomach. The concentration of 1080 in the muscle tissue was related to the administered dosages. Correlation analyses of dosages and residue levels in coyote muscle tissue showed a correlation coefficient of 0.99 for 1080 administered by gavage, and 0.88 for 1080 administered by bait. A correlation coefficient of 0.99 was observed between dosages and mean residues in the breast muscle tissues of magpies. The average CV value was 3.5% for duplicate analyses of 1 g samples of magpie tissues.

PMID: 6746478 [PubMed - indexed for MEDLINE]


Vet Hum Toxicol 1984;26 Suppl 2:29-32

Acute renal failure caused by acute monofluoroacetate poisoning.

Chung HM.

NaFA produces toxic effects by metabolic conversion to fluorocitrate, inhibits Krebs' cycle and the formation of ATP, reduces energy supply to cells, and thus causes cellular dysfunction or degeneration. All body cells are potentially affected, although with different sensitivity. Acute renal failure was found in three out of our five cases, and two were in frank uremia. The ARF was reversible and may be either oliguric or non-oliguric. The causes of ARF were not apparent, but direct nephropathy or some other factors might be involved in the pathogenesis of ARF.

PMID: 6523725 [PubMed - indexed for MEDLINE]


No Abstract available

Bull Environ Contam Toxicol 1983 Dec;31(6):692-8

Acute and sublethal effects of 1080 on starlings.

Balcomb R, Bowen CA 2nd, Williamson HO.

PMID: 6661583 [PubMed - indexed for MEDLINE]


J Toxicol Clin Toxicol 1983 Mar;20(1):85-92

Computed tomography demonstration of brain damage due to acute sodium monofluoroacetate poisoning.

Trabes J, Rason N, Avrahami E.

The case reported developed an acute brain syndrome, including cerebellar signs, shortly after the ingestion of sodium monofluoroacetate. After insiduous improvement of the clinical symptoms, the patient remained with an "end-stage" cerebellar ataxia for 18 months following the acute intoxication. The development of brain atrophy, proven by computed tomography, is considered to represent a direct influence of sodium monofluoroacetate on the brain and to reflect the unique disturbances in cellular metabolism of glucose.

PMID: 6887303 [PubMed - indexed for MEDLINE]


Brain Res 1981 Apr 6;210(1-2):311-22

Ammonia and disinhibition in cat motor cortex by ammonium acetate, monofluoroacetate and insulin-induced hypoglycemia.

Raabe WA.

Ammonia intoxication abolished the suppression of action potential generation by cortical postsynaptic inhibition due to the inactivation of neuronal Cl- extrusion. The disinhibition by ammonia intoxication occurred when ammonia concentrations in the cerebral cortex were increased to 320% of normal. Fluoroacetate poisoning and insulin-induced hypoglycemia, which are known to increase ammonia concentrations in the CNS and previously have been shown to inactivate Cl- extrusion in spinal motoneurons, abolished the suppression of action potential generation by cortical postsynaptic inhibition like ammonia intoxication. This disinhibition occurred at unchanged cerebral ammonia concentrations. The effect of fluoroacetate and insulin induced hypoglycemia on cortical postsynaptic inhibition is either due to a direct, i.e. not ammonia mediated, inactivation of neuronal Cl- extrusion or due to a disturbance of the synaptic mechanisms mediated by the transmitter of cortical inhibition, GABA. Toxic-metabolic encephalopathies which increase cerebral ammonia concentrations beyond 320% of normal may produce a dysfunction of the CNS due to inactivation of neuronal Cl- extrusion leading to ineffective cortical inhibition. However, in fluoroacetate poisoning and insulin-induced hypoglycemia increased ammonia concentrations in the CNS have only a secondary role in initiating a dysfunction of the CNS since disinhibition occurs before ammonia concentrations increase.

PMID: 7013903 [PubMed - indexed for MEDLINE]

From Toxline at Toxnet

Toxicology and Applied Pharmacology, Vol. 56, No. 2, pages 216-220, 17 references, 1980

Evaluation Of The Role Of Ionized Calcium In Sodium Fluoroacetate ("1080") Poisoning

Roy (Shapira) A, Taitelman U, Bursztein S

The role of ionized calcium (7440702) in toxicity induced by sodium-fluoroacetate (62748) was studied in cats. Twelve adult cats were cannulated at the femoral artery to monitor direct blood pressure. A catheter was inserted into the inferior vena cava for exposure to sodium-fluoroacetate at 3 milligrams per kilogram. Electrocardiographic (ECG) measurements were continuously monitored. Blood was sampled at various times, and concentrations of ionized calcium were determined. Forty minutes after poisoning with sodium-fluoroacetate, blood ionized calcium decreased significantly from 1.09 to 0.79 millimolar concentrations in all cats exposed to the compounds. Concomitant with the drop in ionized calcium, a prolongation of the interval in the ECG pattern was seen. Treatment with calcium-chloride (10043524) significantly prolonged the life spans of the treated cats as compared to the control cats. The authors conclude that manifestations of sodium-fluoroacetate poisoning may be correlated with changes in blood ionized calcium concentrations.

From Toxline at Toxnet

Toxicology Letters, Vol. 6, No. 2, pages 67-70, 11 references, 1980

Environmental Temperature, A Factor Modifying The Acute Toxicity Of Organic Solvents, Heavy Metals, And Agricultural Chemicals

Nomiyama K, Matsui K, Nomiyama H

The effects of environmental temperature on the acute toxicity of organic solvents, heavy metals, and agricultural chemicals were studied in 4 week old male ICR-JCL-mice. The organic solvents tested were benzene (71432), toluene (108883), and trichloroethylene (79016). Copper-sulfate (7758987), chromium-trioxide (1333820), mercuric-chloride (7487947), and cadmium-chloride (10108642) were the heavy metals tested, and fratol (62-74-8), methylparathion (298000), and dieldrin (60571) were the agricultural chemicals tested. Animals were acclimatized to an environmental temperature of 8, 22, or 38 degrees-C for 4 weeks, with relative humidity kept at 80, 50, and 27 percent, respectively. Animals were then treated with varying doses of the compounds and median lethal doses for each of the compounds at each environmental atmosphere were determined. The acute toxicities of benzene, trichloroethylene, mercuric-chloride, fratol, methylparathion, and dieldrin were strongest at the environmental temperature of 8 degrees, and these toxicities were followed by those at 38 degrees, with the exception of fratol. Toluene, copper-sulfate, and chromium-trioxide showed the strongest toxicities at 38 degrees, which were followed by those at 8 degrees. The authors conclude that the effects of environmental temperature on the acute toxicity of organic solvents, heavy metals, and agricultural chemicals should be studied further.


Toxicology 1979 Dec;15(1):43-53

Inorganic and organic fluoride concentrations in tissues after the oral administration of sodium monofluoroacetate (Compound 1080) to rats.

Egekeze JO, Oehme FW.

Male rats were used to study the inorganic (ionic) and organic fluoride concentrations in plasma, liver, kidneys and stomach content after oral doses of 0, 2.2, 3.5, 4.0, 5.0 and 7.0 mg sodium monofluoroacetate (SMFA, Compound 1080)/kg body weight. Tissue and plasma ionic fluoride concentrations were observed to be higher in all rats given SMFA as compared to rats in the control group. This observation suggests in vivo defluorination of SMFA. Homogenates of liver obtained from SMFA poisoned rats showed significant increases in ionic fluoride concentration during a 6-day storage period at +4 degrees C, with the total fluoride concentration (ionic and organic) remaining constant. The average percentages of distribution of SMFA (organic fluoride) in plasma, liver, and kidneys were 7.05, 5.07 and 1.68, respectively. Plasma and tissue SMFA concentrations were generally lower than the corresponding stomach fluid SMFA concentrations for all dosage groups. Lethal concentration of SMFA in the liquid stomach content was in the range 84.9--189 micrograms/ml, corresponding to total (ionic and organic) fluoride concentrations in the range of 16.1--36 micrograms/ml.

PMID: 542959 [PubMed - indexed for MEDLINE]


J Reprod Fertil 1979 May;56(1):201-7

Effects of fluoroacetate on the testis of the rat.

Sullivan JL, Smith FA, Garman RH.

Rats recieving 20, 6.6 or 2.2 p.p.m. sodium fluoroacetate in the drinking water were killed daily during the 7 days of treatment and at more widely spaced intervals in the succeeding 21 days. Testicular weight and ATP concentrations decreased in rats receiving 20 or 6 p.p.m. fluoroacetate, while citrate concentrations were elevated and morphological damage was seen in the testes of all the treated rats. Initial cellular changes common to the three treatment groups included altered appearance and decreased numbers of spermatids, and formation of spermatid and spermatocyte giant cells. At the two higher concentrations damage progressed to marked seminiferous tubule atrophy. Regeneration of the seminiferous tubules was complete by 7 days after treatment, in the rats given 2 p.p.m. but regeneration was not complete by Day 21 after treatment in those receiving the higher doses. Spermatogenesis was abnormal in some instances during the regneration period in these groups. The findings are consistent with impaired energy production via blockage of the Krebs cycle, and subsequent impairment of carbohydrate metabolism through the Embden-Meyerhof pathway.

PMID: 469843 [PubMed - indexed for MEDLINE]

From Toxline at Toxnet

Audobon 80(2): 53-58, 62, 68, 72-74, 76-78, 82, 86-87 1978

Last days of the condor?

McNulty F

PESTAB. An overview of the threat to wild condors of the San Joaquin Valley from the use of pesticides or the disturbance of the environment by hunters or dams is given. In 1950, DDT was sprayed on 150,000 acres of rangeland adjacent to the western borders of the valley. More recently, herbicides have been used extensively on hundreds of acres to control brush and convert native vegetation to pastureland in the valley. Much of the valley is now cultivated for the growth of crops, and the various types of agricultural chemicals used in conjunction with farming often permeate the air and water. The chemical 1080 (sodium monofluoroacetate) is also used on private grounds near places where condors forage. Condors often feed on carcasses containing high levels of pesticides, such as 1080 and strychnine, which are used extensively for rodent control in the San Joaquin Valley. In 1965, the analysis of the corpse of an immature condor showed residues of 18 ppm DDT and 30 ppm DDE in the visceral fat. Residues of 1080 were also found in the digestive tract of the bird. Many efforts that have been made to save the condor populations from the harmful effects of chemical and physical environmental stresses are discussed.


Am J Dis Child 1975 Oct;129(10):1224-6

Sodium fluoroacetate poisoning.

Reigart JR, Brueggeman JL, Keil JE.

We observed a case of poisoning with sodium fluoroacetate, an extremely lethal rodenticide that has had relatively strict controls placed on its use. The case was unusual in the very long time the rodenticide had been present in the home, the mild nature of the poisoning, and the remarkably delayed onset of serious central nervous system symptoms. It demonstrates the need for even stronger controls on the use of sodium fluoroacetate.

PMID: 1190148 [PubMed - indexed for MEDLINE]


Folia Biol (Praha) 1975;21(4):244-9

Inhibition of DNA synthesis in mouse lymphosarcoma LS/BL cells by fluorocitrate.

Novak L, Juraskova V.

Fluorocitrate is a specific inhibitor of aconitase activity (EC It causes an inhibition of citric acid cycle reactions and consequently reduces the oxygen consumption, as well as the total volume of oxidative phosphorylations. Experiments using 3H-thymidine incorporation into mouse lymphosarcoma LS/BL cells proved that the in vitro blocking of citric acid cycle by fluorocitrate (3.6 and 7.2 mM) was accompanied by a decrease in DNA synthesis by 40 to 60 percent, as compared to control cells. A similar inhibitory effect upon DNA synthesis was also found in cells cultured in the abdominal cavity of host mice injected intraperitoneally with 5 mg./kg. of sodium fluoroacetate. Following the injection, fluorocitrate is formed in vivo by way of Peters' lethal synthesis.

PMID: 1242379 [PubMed - indexed for MEDLINE]

From Dart Special at Toxnet

TERATOLOGY 7:127-134,1973



Taxonomic Name: RATTUS, WISTAR
Test Object: MAMMAL, RAT

Name of Agent (CAS RN):
2-DEOXY-D-GLUCOSE ( 154-17-6 )

Assay Method:


J Neurochem 1972 Sep;19(9):2107-18

No Abstract available

Effects of sodium fluoroacetate on the metabolism of N-acetylaspartate and aspartate in mouse brain.

Nadler JV, Horwitch P, Cooper JR.

PMID: 5072387 [PubMed - indexed for MEDLINE]


Dokl Akad Nauk SSSR 1972 Jun 1;204(4):1013-6

No Abstract available

[Effect of electrolytic destruction of non-specific structures of the anterior thalamus on the formation of convulsive phenomena during sodium fluoroacetate poisoning]

[Article in Russian]

Kirzon MV, Titov SA.

PMID: 5042378 [PubMed - indexed for MEDLINE]

From Dart Special at Toxnet

TERATOLOGY 4:501,1971



Taxonomic Name: RATTUS
Test Object: MAMMAL, RAT

Name of Agent (CAS RN):
2-DEOXY-D-GLUCOSE ( 154-17-6 )

Assay Method:

From Toxline at Toxnet

Med. J. Aust.; VOL 2 ISS Oct 3 1970, P641-642, (REF 2)

Poisoning due to sodium fluoroacetate (1080)

McTaggart DR

12 High Street, Burnie, Tasmania, Australia

A case is described of poisoning in a boy who ingested wheat previously impregnated with 1080 (sodium fluoroacetate) to poison rabbits. The product causes vomiting, convulsions, coma, respiratory depression and cardiac irregularities. The boy was treated for convulsions with I.V. thiopentone sodium and diazepam. He was resuscitated from cardiac arrest but was left with severe neurological impairment. 1080 is a widely used agricultural poison with cardiotoxic and neurotoxic effects and stingent precautions exist to control its use.

From Toxline at Toxnet

Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 67, No. 4, pages 69-73, 9 references, 1969

Combined Electrical Activity Of Some Subcortical Structures In The Brain Of Albino Rats At Various Stages Of Sodium Fluoroacetate Poisoning

Artyushkova VA, Kirzon MV, Timeiko VN

The effect of sodium-fluoroacetate (62-74-8) on electrical activity in the brain was investigated in rats. Electrical activity was recorded in the reticular nucleus of the thalamus and in the caudate nucleus of male albino-rats using bipolar electrodes. Twenty four hours after electrode implantation, animals were dosed intraperitoneally with sodium-fluoroacetate at 5 milligrams per kilogram. At various times thereafter, the complete electrical activity was recorded in selected brain structures using a loop oscillograph. The electrical activity was summed with an integrator enabling relative changes in complete electrical activity to be detected. Readings were taken for 5 minutes, every 15 minutes. Control animals showed characteristic slow waves, 4 to 6 per second, mainly in the reticular nucleus of the thalamus throughout the 6 hour experiment. Upon sodium-fluoroacetate treatment, slow waves were recorded and later faster waves, 12 to 15 per second, superceded the slow waves. At the end of the first hour and thereafter waves of slow frequency disappeared and those of faster frequency prevailed. Later, the frequency and amplitude of waves increased, particularly pronounced in the period of paroxysms in the reticular nucleus of the thalamus. After 3 hours, the fast waves were depressed and the complete electrical activity was not reversible. The authors conclude that the increase in complete electrical activity after the initial stage reflects participation of the central nervous system in compensatory processes evoked by deepening hypothermia and anoxia caused by sodium-fluoroacetate poisoning. (Russian)

From Science Direct

Life Sciences; Volume 3, Issue 7 , July 1964, Pages 709-713

An approach to the biochemical study of teratogenic substances on isolated rat embryo

R. De Meyer and J. De Plaen

Laboratoire de Recherches de la Clinique Medicale, Hospital Saint-Pierre, Louvain, Belgium

1. Embryonic tissue produces more CO2 from glucose-1-C14, and less from acetate, than does liver tissue.
2. More glucose is probably disposed of via the pentose phosphate shunt by the embryo than by normal liver tissue.
3. Carbutamide, 2-deoxyglucose and sodium fluoroacetate cause a depression of several measured metabolic parameters of embryos

Comments from Dart Special at Toxnet:
Taxonomic Name: RATTUS
Test Object: MAMMAL, RAT
Name of Agent (CAS RN):
CARBUTAMIDE ( 339-43-5 )
2-DEOXYGLUCOSE ( 61-58-5 )

From Science Direct

Tetrahedron; Volume 5, Issue 1 , 1959, Pages 38-43

Rupture of the C–F link by alkali and other reagents*

P. Mirosevic-Sorgo and B. C. Saunders

University Chemical Laboratory, Lensfield Rd., Cambridge U.K.

The reactivity of the carbon-fluorine bond in certain -fluorocarboxylic acids and esters with respect to nucleophilic attack has been examined. Heating under reflux with 30 per cent sodium hydroxide hydrolyses this type of compound and on this basis a method of fluorine analysis is suggested.
Phenyl magnesium bromide converts methyl fluoroacetate and fluoroacetyl chloride into 1:2:2-triphenylethanol. The so-called unreactive fluorine atom in methyl -fluorobutyrate is also removed by this reagent giving 2:2-diphenyltetrahydrofuran.

*1 Part IX, J. Chem. Soc. 1929 (1953).

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