From
TOXNET
Journal
of Applied Animal Research 1992;2(2):81-5
Embryotoxic
and teratogenic effects of flocoumafen in chick embryos
and white rats.
Khalifa
BA, Salem FM, Menha MA
Department
of Pharmacology and Forensic Medicine, Faculty of
Veterinary Medicine, Cairo University, Egypt.
Abstract:
Embryotoxic and teratogenic effects of flocoumafen
(new anticoagulant rodenticide) in chick embryos and
white rats were studied. Flocoumafen was injected
(2 ug/egg) to the yolk sac of Fayuomi fertile eggs
on the 5th and 9th day of incubation. It was orally
administered to pregnant female rats (2.5 and 5 ug/kg
B. Wt.) on the 8th, 10th and 12th day of gestation.
The study revealed that flocoumafen
was more embryotoxic than teratogenic in both chick
embryos and white rats.
|
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15091419
Environ Pollut. 1996;91(3):279-82.
Second-generation rodenticides and
polecats (Mustela putorius) in Britain.
Shore RF, Birks JD, Freestone P, Kitchener
AC.
NERC, Institute of Terrestrial Ecology, Monks Wood, Abbots
Ripton, Huntingdon, Cambridgeshire, PE17 2LS, UK.
In Britain, polecats Mustela putorius hunt around farm buildings,
especially in winter, and, as a result, may be secondarily
exposed to rodenticides by eating contaminated prey. This
paper reports the first survey of second-generation rodenticides
in polecats. Twenty-nine adult polecats which had been killed
either accidentally on roads (24) and in traps (4), or had
died of an unknown cause (1) were collected during 1992-1994.
The livers of 24 animals and the stomach walls of the remaining
five, for which the livers were not available, were analysed
for difenacoum, bromadiolone, brodifacoum and flocoumafen.
In total, rodenticide residues were detected in 31% of the
polecats analysed. Residues were found in seven of the 24
livers (29%) and in two of the five stomachs analysed (40%).
Difenacoum was detected most frequently (28% of animals),
and was the only rodenticide in the stomach, while bromadiolone
and brodifacoum were detected in only 10% and 3% of polecats,
respectively. Flocoumafen was not detected in any animals.
More than one rodenticide occurred in the livers of two animals;
one contained difenacoum and bromadiolone, the other also
contained brodifacoum. There was no sex bias in the proportion
of animals containing rodenticides. Animals with detectable
residues came from more than one county and were collected
only during January-April in each year.
PMID: 15091419 [PubMed - in process]
From
TOXNET
INT BIODETERIOR
BIODEGRAD; 30 (1). 1992.
65-76.
Laboratory
evaluation of the toxicity of flocoumafen as a single-feed
rodenticide to seven rodent species.
GILL
JE
Central
Sci. Lab., Ministry Agric., Fisheries Food, Slough Lab., London
Rd., Slough, Berkshire SL3 7HJ, UK.
Abstract:
BIOSIS COPYRIGHT: BIOL ABS. Laboratory feeding tests were
carried out to determine the toxicity of the anti-coagulant
flocoumafen to three universal commensal rodent pest species,
Rattus norvegicus (Berk.), R. rattus, L. and Mus domesticus
(Marshall and Sage) and four tropical rodent species not native
to UK, Meriones shawi (Duvernoy), Acomys cahirinus (Desmarest),
Arvicanthis niloticus (Desmarest) and Mesocricetus auratus
(Waterhouse). In the 1-day no-choice tests, flocoumafen gave
97.5% mortality of warfarin-resistant laboratory rats, 100%
mortality of difenacoum-resistant rats, 92% mortality of R.
rattus, 75% mortality of warfarin-resistant M. domesticus,
and 100% mortality of A. niloticus. In the choice test, flocoumafen
was generally palatable and gave 100% mortality of warfarin-resistant
and susceptible R. norvegicus, and warfarin-susceptible R.
rattus, but only 65% mortality was obtained with warfarin-resistant
M. domesticus and 60% mortality of A. niloticus. Flocoumafen
at 0 005% (w/w) as a [abstract truncated]
From
TOXNET
Archives
of Toxicology, Supplement 14, pages 160-165, 7 references,
1991 [NIOSH]
Metabolic
and Toxicological Studies on the Anticoagulant Rodenticide,
Flocoumafen
Veenstra
GE, Owen DE, Huckle KR
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1805726&dopt=Abstract
Arch
Toxicol Suppl 1991;14:160-5
Metabolic
and toxicological studies on the anticoagulant rodenticide,
flocoumafen.
Veenstra GE, Owen DE, Huckle
KR.
Health, Safety and Environment Division, Shell
Internationale Petroleum Maatschappij, The Hague, The
Netherlands.
PMID: 1805726 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2756717&dopt=Abstract
Xenobiotica
1989 Jan;19(1):51-62
Studies
on the fate of flocoumafen in the Japanese quail (Coturnix
coturnix japonica).
Huckle KR, Warburton PA, Forbes
S, Logan CJ.
Shell Research
Ltd, Sittingbourne Research Centre, Kent, UK.
1. 14C-Flocoumafen, administered to Japanese
quail as a single oral or i.p. dose, was rapidly and extensively
eliminated in excreta; most was eliminated within 24 h. Extensive
metabolism of the rodenticide was seen, with at least 8 metabolites
detected; unchanged flocoumafen comprised 9% dose. The elimination
kinetics and metabolic profiles were qualitatively similar
after oral and i.p. dosing.
2. The major metabolites (60% dose) were labile to beta-glucuronidase,
liberating aglycones with identical chromatographic mobilities
to those of the unchanged flocoumafen isomers.
3. Radioactivity was retained mostly in the liver; largely
as unchanged flocoumafen associated with the mitochondrial
and microsomal fractions. Elimination of radioactivity from
most tissues was biphasic with an initially rapid depletion
(5 days) followed by a slow terminal elimination phase. The
elimination half life from liver was greater than 100 days.
4. Livers of quail receiving extended dietary exposure to
flocoumafen at 5, 15 and 50 ppm had concentrations of flocoumafen
(1.0 nmol/g) that were independent of dose, indicating a capacity-limited
binding site. These hepatic concentrations were similar to
those after a single oral dose and were also similar to those
in rats. The data indicate the presence in quail liver of
a saturable high affinity flocoumafin binding site with similar
characteristics and capacity to that in the rat.
5. The selective toxicity of flocoumafen
to rats (highly toxic) and quail (moderately toxic)
appears to arise from differences in metabolism rather than
from anticoagulant binding in the liver. When
hepatic binding sites of rats are saturated anticoagulant
action becomes lethal, whereas quail are able to survive
and extensively metabolize the compound.
PMID: 2756717 [PubMed - indexed for MEDLINE]
From
TOXNET
DAN VETERINAERTIDSSKR;
72 (19).
1989. 1119-1123.
[Language:
Danish]
ACCIDENTAL
RODENTICIDE POISONING OF DOMESTIC ANIMALS IN 1988
BILLE
N, LUND M
BIOSIS
COPYRIGHT: BIOL ABS. RRM DOG CAT ANTICOAGULANT AGENT
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3245237&dopt=Abstract
Xenobiotica
1988
Dec;18(12):1465-79
Elimination
and accumulation of the rodenticide flocoumafen in rats following
repeated oral administration.
Huckle KR, Hutson DH, Warburton
PA.
Shell Research,
Ltd., Sittingbourne Research Centre, Kent, UK.
1. Following multiple oral administration of
14C-flocoumafen to rats at 0.02 and 0.1 mg/kg per week, appreciable
cellular accumulation was seen in the liver.
2. Residues in the liver increased with dose throughout the
duration of the experiment (14 weeks) at the low dose, but
reached a plateau after 4 weeks at the high dose. The major
component was unchanged flocoumafen together with a minor
polar metabolite seen also in faeces.
3. The data suggest the presence in rat liver of a saturable
high-affinity binding site for flocoumafen and a second binding
site of lower affinity.
4. Lethal anticoagulant action occurs only when the binding
sites have become saturated.
5. A range of haematological and clinical chemistry measurements
failed to predict the onset of anticoagulant toxicity seen
in the high dose treatment group.
6. Flocoumafen was not extensively metabolised; at the low
dose, approximately 30% of the cumulative administered dose
was eliminated in the faeces within 3 days of each dosing,
mainly as unchanged rodenticide. At the high dose, this value
ranged from 18% after the first dose to 59% after the tenth
dose.
7. Two more polar metabolites and a lipophilic compound were
minor products in faeces. Amounts of the polar products increased
with cumulative dosage received. The urinary route of elimination
was a very minor one (less than 1.6%) at both doses.
PMID: 3245237 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3841547&dopt=Abstract
J
Hyg (Lond) 1985
Dec;95(3):623-7
Pen
and field trials of a new anticoagulant rodenticide flocoumafen
against the house mouse (Mus musculus L.).
Rowe FP, Bradfield A, Swinney
T.
The efficacy of flocoumafen, a novel anticoagulant rodenticide,
was evaluated in feeding tests on confined and free-living
populations of house mice (Mus musculus L.). In four pen trials,
family groups of laboratory-reared wild mice were conditioned
to feeding on plain foods and then offered flocoumafen at
0.005% in pinhead oatmeal bait. All 68 mice, comprising juvenile
and adult animals, died within 10 days. Ten field trials were
carried out, using the same formulated poison bait, against
mice infesting farm buildings. Mean treatment success, estimated
from live-capture and mortality data, ranged between 87.1
and 100%. The performance of flocoumafen is compared with
that of difenacoum, bromadiolone and brodifacoum used at the
same concentration in oatmeal bait. Flocoumafen gave an equally
effective but quicker kill of mice. It is concluded that flocoumafen
is a promising new rodenticide for the control of M. musculus.
PMID: 3841547 [PubMed - indexed for MEDLINE]
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