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
(mg/kg) |
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 |
Mouse
|
Yakkyoku
1977 |
oral |
0.1 |
0.7
mg/m |
0.07
mg/m3 |
REFERENCES:
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.
http://www.cdc.gov/niosh/idlh/62748.html
|
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12377993
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. |
1997
- THE TOXICITY OF SODIUM TRIFLUOROACETATE
TO ALGAE, WITH COVER LETTER DATED 3/17/1997
SOLVAY
DUPHAR B.V.
Order
Number: NTIS/OTS0558955
Source: EPA/OTS; Doc #86970000745 |
Keywords:
AFEAS
SODIUM TRIFLUOROACETATE (2923-18-4); *
ENVIRONMENTAL EFFECTS
PLANT GROWTH OR DAMAGE TESTS
ALGAE
PHARMACO KINETICS
ECOSYSTEM MODELING
ENVIRONMENTAL FATE
BIOCONCENTRATION/BIOACCUMULATION
CAS
Registry Numbers:
62-74-8
381-73-7
2923-18-4 |
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. |
1995
- COMPARISON OF THE TOXICITY OF
SODIUM TRIFLUOROACETATE, DIFLUOROACETIC ACID, SODIUM MONOFLUOROACETATE
& SODIUM FLUORIDE TO THE ALGA WITH COVER LETTER DATED
05/12/95
SOLVAY
DUPHAR
Order Number: NTIS/OTS0572560
EPA/OTS;
Doc #86950000254 |
Keywords:
AFEAS
SODIUM TRIFLUOROACETATE (CAS# 2923-18-4)
ENVIRONMENTAL EFFECTS
ACUTE TOXICITY
ALGAE
CAS
Registry Numbers:
62-74-8
381-73-7
1333-83-1
2923-18-4 |
1995
- COMPARISON OF THE TOXICITY OF
SODIUM TRIFLUOROACETATE, SODIUM DIFLUOROACETATE, SODIUM
MONOFLUOROACETATE AND SODIUM FLUORIDE TO THE ALGA WITH
COVER LETTER DATED 05/12/95
SOLVAY
DUPHAR
Order Number: NTIS/OTS0572561
EPA/OTS; Doc #86950000255 |
Keywords:
AFEAS
SODIUM TRIFLUOROACETATE (CAS# 2923-18-4)
ENVIRONMENTAL EFFECTS
ACUTE TOXICITY
ALGAE
CAS
Registry Numbers:
62-74-8
381-73-7
1333-83-1
2923-18-4 |
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.
Keywords:
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.
Keywords:
Environmental surveys
Pesticides
Toxicology
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.
Keywords:
Environmental surveys
Pesticides
Toxicology
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.
Keywords:
Environmental surveys
Pesticides
Toxicology
Fluoroacetamide
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 |
Keywords:
Sodium compounds
Poisoning
Acetates |
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15261984
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15206584
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15063312
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12517149
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12125587&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11931513&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11929699&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12505362
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]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12600049
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10762315&dopt=Abstract
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.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10413241&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9870987&dopt=Abstract
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.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9595190&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8941201&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7663087&dopt=Abstract
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
Pesticides.
Schardein JL
International Research and Development Corporation, Mattawan,
MI.
Medical Subject Headings (MeSH):
Pregnancy
Animal
Human
Female
Pesticides/*TOXICITY
*Abnormalities, Drug-Induced
2,4,5-Trichlorophenoxyacetic Acid/TOXICITY
Insecticides/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)
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1609740&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1626884&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2073603&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2128162&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2673373&dopt=Abstract
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:
PMID: 2673373
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2633850&dopt=Abstract
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.
Abstract
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.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3391967&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3382787&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3580616&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3592762&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2884018&dopt=Abstract
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.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3722090&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3778356&dopt=Abstract
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
www.cogsci.princeton.edu/cgi-bin/webwn
From Dart Special at Toxnet
DISS ABSTR INT B 46:1497,1986
DEVELOPMENT OF DIETARY LC50 AND REPRODUCTION
TEST PROTOCOLS USING MINK AND FERRETS AS REPRESENTATIVE MAMMALIAN
CARNIVORES
HORNSHAW TC
Taxonomic Name:
MUSTELA VISON
MUSTELA FURO
Test Object: MAMMAL, MINK
MAMMAL, FERRET
Name of Agent (CAS RN):
SODIUM MONOFLUOROACETATE ( 62-74-8 )
O-CRESOL ( 95-48-7 )
THIRAM ( 137-26-8 )
AROCLOR 1254 ( 11097-69-1 )
Assay Method:REPRODUCTIVE TOXICITY
Route of Administration: PER ORAL DIET
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3976163&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6746478&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6523725&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6661583&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6887303&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7013903&dopt=Abstract
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.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=542959&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=469843&dopt=Abstract
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.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1190148&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1242379&dopt=Abstract
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 4.2.1.3). 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
INFLUENCE OF 2-DEOXY-D-GLUCOSE AND SODIUM
FLUOROACETATE ON RESPIRATORY METABOLISM OF RAT EMBRYOS DURING
ORGANOGENESIS
SPIELMANN H, MEYER-WENDECKER R, SPIELMANN
F
Taxonomic Name: RATTUS, WISTAR
Test Object: MAMMAL, RAT
Name of Agent (CAS RN):
2-DEOXY-D-GLUCOSE ( 154-17-6 )
SODIUM FLUOROACETATE ( 62-74-8 )
Assay Method:
BIOCHEMISTRY AND METABOLISM
GROWTH
MUSCULOSKELETAL SYSTEM
EXTRA-EMBRYONIC STRUCTURES
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=5072387&dopt=Abstract
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=5042378&dopt=Abstract
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
INFLUENCE OF DIFFERENT METABOLIC INHIBITORS
ON THE RESPIRATION OF RAT EMBRYOS IN VITRO
SPIELMANN H, LUECKE I, MEYER-WENDECKER R, WEHMANN F
Taxonomic Name: RATTUS
Test Object: MAMMAL, RAT
Name of Agent (CAS RN):
2-DEOXY-D-GLUCOSE ( 154-17-6 )
SODIUM FLUOROACETATE ( 62-74-8 )
Assay Method:
RESPIRATORY STUDY
BIOCHEMISTRY AND METABOLISM
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
Abstract
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 )
SODIUM FLUOROACETATE ( 62-74-8 )
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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