Online
December 2004 at http://www.dse.murdoch.edu.au/research/interests/details/7853
Honours
Projects
Associate
Professor Robert Mead
Murdoch University, Perth, Western Australia
Position:
Assoc Prof in Biol (Biochemistry)
Research
Toxicology and metabolism of fluorinated pesticides
particularly fluoroacetate and 1,3 difluoro-2-propanol.
Development of antidotes to combat accidental ingestion
of toxins. Mode of toxic action of plant secondary compounds
particularly in relation to plant-animal interaction.
Projects
Metabolism and Toxicology of the
Pesticide, Gliftor
Gliftor is a pesticide currently
used in the former USSR to control small rodents such
as voles. It is a mixture of 70% 1,3 difluoro-2-propanol
and 30% 3-chloro-1-fluoro-2-propanol. Our recent work
has established that it is toxic because it is metabolised
in the poisoned animal to fluoroacetate, a pesticide
used in Australia to control rabbits. The toxicity
of fluoroacetate is the result of its conversion into
fluorocitrate which is a potent inhibitor of the TCA-cycle-enzyme,
aconitase. We have determined that 1,3 difluoro-2-propanol
is initially converted in the animal to difluoroacetone
by an NAD+-dependent alcohol dehydrogenase and this
metabolite is then converted to fluoroacetate and hence
fluorocitrate. We have also established that the NAD+-dependent
alcohol dehydrogenase is powerfully inhibited in vivo
and in vitro by pyrazole, diethyldithio-carbamate and
by 4 methyl pyrazole. These compounds, therefore, prevent
the conversion of 1,3 difluoro-2-propanol to fluorocitrate
and can function as effective antidotes in vivo, to
combat accidental ingestion of the pesticide. The toxic
properties and metabolic fate of the minor component
of Gliftor (3chloro-1-fluoro-2-propanol) are unknown
and are currently being investigated. Techniques to
be employed will include citrate and fluoride assays;
determination of aconitase and cytochrome P450 activity
in kidney and liver homogenates and analysis of incubation
mixtures by gas-liquid chromatography and mass spectrometry.
|
| "Toxicometric
Parameters of Industrial Toxic Chemicals Under Single Exposure,"
Izmerov, N.F., et al., Moscow, Centre of International Projects,
GKNT, 1982, Vol. -, Pg. 71, 1982. (From ChemIDplus at Toxnet) |
Organism |
Test
Type |
Route |
Reported
Dose (Normalized Dose) |
mammal
(species unspecified) |
LD50 |
oral |
165mg/kg
(165 mg/kg) |
mouse |
LC50 |
inhalation |
1260mg/m3/2H
(1260 mg/kg) |
mouse |
LD50 |
oral |
165mg/kg
(165 mg/kg) |
rabbit |
LD50 |
oral |
7600ug/kg
(7.6 mg/kg) |
rat |
LC50 |
inhalation |
580mg/m3/4H
(580 mg/kg) |
rat |
LD50 |
oral |
96mg/kg
(96 mg/kg) |
rat |
LD50 |
skin |
66mg/kg
(66 mg/kg) |
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]
Note from FAN:
Three of the pesticides noted above are fluorinated. Tetramine
is iodinated - its molecular formula is: C16-H34-N2.2I. -EC.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11170315
J Biochem Mol Toxicol. 2001;15(1):47-54.
The mode of toxic action of the pesticide
gliftor: the metabolism of 1,3-difluoroacetone to (-)-erythro-fluorocitrate.
Menon KI, Feldwick MG, Noakes PS, Mead
RJ.
School of Biological Sciences and Biotechnology, Murdoch University,
Western Australia.
The biochemical toxicology of 1,3-difluoroacetone, a known
metabolite of the major ingredient of the pesticide Gliftor
(1,3-difluoro-2-propanol), was investigated in vivo and in vitro.
Rat kidney homogenates supplemented with coenzyme A, ATP, oxaloacetate,
and Mg2+ converted 1,3-difluoroacetone to (-)-erythro-fluorocitrate
in vitro. Administration of 1,3-difluoroacetone (100 mg kg(-1)
body weight) to rats in vivo resulted in (-)-erythro-fluorocitrate
synthesis in the kidney, which was preceded by an elevation
in fluoride levels and followed by citrate accumulation. Animals
dosed with 1,3-difluoroacetone did not display the 2-3 hour
lag phase in either (-)-erythro-fluorocitrate synthesis or in
citrate and fluoride accumulation characteristic of animals
dosed with 1,3-difluoro-2-propanol. We demonstrate that the
conversion of 1,3-difluoro-2-propanol to 1,3-difluoroacetone
by an NAD+-dependent oxidation is the rate-limiting step in
the synthesis of the toxic product, (-)-erythro-fluorocitrate
from 1,3-difluoro-2-propanol. Prior administration of 4-methylpyrazole
(90 mg kg(-1) body weight) was shown to prevent the conversion
of 1,3-difluoro-2-propanol (100 mg kg(-1) body weight) to (-)-erythro-fluorocitrate
in vivo and to eliminate the fluoride and citrate elevations
seen in 1,3-difluoro-2-propanol-intoxicated animals. However,
administration of 4-methylpyrazole (90 mg kg(-1) body weight)
to rats 2 hours prior to 1,3-difluoroacetone (100 mg kg(-1)
body weight) was ineffective in preventing (-)-erythro-fluorocitrate
synthesis and did not diminish fluoride or citrate accumulation
in vivo. We conclude that the prophylactic and antidotal properties
of 4-methylpyrazole seen in animals treated with 1,3-difluoro-2-propanol
derive from its capacity to inhibit the NAD+-dependent oxidation
responsible for converting 1,3-difluoro-2-propanol to 1,3-difluoroacetone
in the committed step of the toxic pathway.
PMID: 11170315 [PubMed - indexed for MEDLINE]
http://www.publish.csiro.au/paper/WR99048.htm
Wildlife Research 27(3) 297 - 300, 2000
Acute toxicity of cholecalciferol and
gliftor baits to the European rabbit, Oryctolagus cuniculus
R. J. Henderson and C. T. Eason
Alternatives to sodium monofluoroacetate (1080) and pindone
are required for control of wild rabbits. The palatability and
toxicity of cereal baits containing either cholecalciferol or
gliftor were assessed on captive domestic rabbits. Although
rabbits showed considerable variation in their individual response
to cholecalciferol, they were very susceptible to the toxicant
(LD50 = 4.4 mg kg–1) and it would be lethal to almost
all rabbits ingesting doses greater than 15 mg kg–1. However,
concentrations of 0.04% and 0.18% cholecalciferol in bait were
not readily eaten by rabbits, suggesting that further research
is required to mask the taste and/or smell of the toxicant.
The LD50 of gliftor in cereal bait to rabbits was 2.2 mg kg–1.
Rabbits showed no measurable aversion
to baits that contained 0.2% w/w gliftor. A lower concentration
of 0.1% gliftor in bait should be tested on wild populations
of rabbits.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9414486
Journal of Biochemical and Molecular Toxicology; 12: 41-52,
1998
The biochemical toxicology of 1,3-difluoro-2-propanol,
the major ingredient of the pesticide Gliftor: The potential
of 4-methylpyrazole as an antidote
M. G. Feldwick (1), P. S. Noakes (1),
U. Prause 1, R. J. Mead (1), P. J. Kostyniak (2)
1School of Biological Sciences and Biotechnology, Murdoch University,
Murdoch 6150, Western Australia
2Toxicology Research Center, University at Buffalo, Buffalo,
NY 14214
Administration to rats of 1,3-difluoro-2-propanol (100 mg kg-1
body weight), the major ingredient of
the pesticide gliftor, resulted in accumulation of citrate
in the kidney after a 3 hour lag phase.
1,3-Difluro-2-propanol was found to be metabolized to 1,3-difluoroacetone
and ultimately to the aconitate hydratase inhibitor (-) erythrofluorocitrate
and free fluoride. The conversion of 1,3-difluoro-2-propanol
to 1,3-difluoroacetone was found to be catalyzed by an NAD+-dependent
alcohol dehydrogenase, while the defluorination was attributed
to microsomal monooxygenase activity induced by phenobarbitone
and inhibited by piperonyl butoxide. 4-Methylpyrazole was found
to inhibit both of these processes in vitro and when administered
(90 mg kg-1 body weight) to rats, 2 hours prior to 1,3-difluoro-2-propanol,
eliminated signs of poisoning, prevented (-) erythrofluorocitrate
synthesis, and markedly decreased citrate and fluoride accumulation
in vivo. 4-Methylpyrazole also appeared to diminish (-) erythrofluorocitrate
synthesis from fluoroacetate in vivo, and this was attributed
to its capacity to inhibit malate dehydrogenase activity. The
antidotal potential of 4-methylpyrazole and the potential for
1,3-difluoro-2-propanol to replace fluoroacetate (compound 1080)
as a vertebrate pesticide is discussed. © 1997 John Wiley
& Sons, Inc. J Biochem Toxicol 12: 41-52, 1998
From
Toxline at Toxnet
ENVIRONMENTAL
SCIENCE & TECHNOLOGY; 31 (9). 1997.
2445-2454.
Fluorinated
organics in the biosphere.
KEY BD, HOWELL RD, CRIDDLE CS
Dep. Civil
Environ. Eng., Mich. State Univ., East Lansing, MI 48824, USA.
BIOSIS COPYRIGHT: BIOL ABS. The use of organofluorine compounds
has increased throughout this century, and they are now ubiquitous
environmental contaminants. Although generally viewed as recalcitrant
because of their lack of chemical reactivity, many
fluorinated organics are biologically active. Several
questions surround their distribution, fate, and effects. Of
particular interest is the fate of perfluoroalkyl substituents,
such as the trifluoromethyl group. Most evidence to date suggest
that such groups resist defluorination, yet they can confer
significant biological activity. Certain volatile fluorinated
compounds can be oxidized in the troposphere yielding nonvolatile
compounds, such as trifluoroacetic acid. In addition, certain
nonvolatile fluorinated compounds can be transformed in the
biosphere to volatile compounds. Research is needed to assess
the fate and effects of nonvolatile fluorinated organics, the
fluorinated impurities present in commercial formulations, and
the transformation
CAS Registry
Numbers:
137938-95-5 - na
112839-33-5 - chlorazifop [C14H11Cl2NO4]
112839-32-4 - chlorazifop [ C14H11Cl2NO4]
106917-52-6 - flusulfamide [C13H7Cl2F3N2O4S]
104040-78-0 - flazasulfuron [C13H12F3N5O5S]
102130-93-8 - 4-Fluorothreonine [ C4-H8-F-N-O3
]
101463-69-8 - flufenoxuron [C21H11ClF6N2O3]
101007-06-1 - acrinathrin [C26H21F6NO5]
97886-45-8 - dithiopyr [C15H16F5NO2S2]
96525-23-4 - flurtamone [C18H14F3NO2]
90035-08-8 - flocoumafen [C33H25F3O4]
88485-37-4 - fluxofenim [C12H11ClF3NO3]
85758-71-0 - 1-Decanol, 1,1,2,2,3,3,4,4,5,5,6,6,7,7,8,8,9,9,10,10,10-heneicosafluoro-
[ C10-H-F21-O ]
83164-33-4 - diflufenican [C19H11F5N2O2]
82657-04-3 - bifenthrin [C23H22ClF3O2]
81613-59-4 - flupropadine [C20H23F6N]
80164-94-9 - Methanone, phenyl((trifluoromethyl)phenyl)-,
dichloro deriv. [ C14-H7-Cl2-F3-O
]
80020-41-3 - furyloxyfen [C17H13ClF3NO5]
79622-59-6 - fluazinam [C13H4Cl2F6N4O4]
79538-32-2 - tefluthrin [C17H14ClF7O2]
77501-63-4 - lactofen [C19H15ClF3NO7]
77501-60-1 - fluoroglycofen [C16H9ClF3NO7]
76674-21-0 - flutriafol [C16H13F2N3O]
72850-64-7 - flurazole [C12H7ClF3NO2S]
72178-02-0 - fomesafen [C15H10ClF3N2O6S]
71422-67-8 - chlorfluazuron [C20H9Cl3F5N3O3]
69806-34-4 - Haloxyfop [C15H11ClF3NO4]
69335-91-7 - fluazifop [C15H12F3NO4]
68694-11-1 - Triflumizole [ C15-H15-Cl-F3-N3-O
]
68085-85-8 - cyhalothrin [C23H19ClF3NO3]
67485-29-4 - hydramethylnon [C25H24F6N4]
66332-96-5 - flutolanil [C17H16F3NO2]
64628-44-0 - triflumuron [C15H10ClF3N2O3]
63333-35-7 - bromethalin [C14H7Br3F3N3O4]
62924-70-3 - flumetralin [C16H12ClF4N3O4]
61213-25-0 - flurochloridone [C12H10Cl2F3NO]
59756-60-4 - fluridone [C19H14F3NO]
57041-67-5 - Desflurane [ C3-H2-F6-O
]
56425-91-3 - flurprimidol [C15H15F3N2O2]
55283-68-6 - ethalfluralin [C13H14F3N3O4]
53780-34-0 - mefluidide [C11H13F3N2O3S]
50594-66-6 - acifluorfen [C14H7ClF3NO5]
42874-03-3 - oxyfluorfen [C15H11ClF3NO4]
40856-07-3 - Difluoromethanesulphonic
acid [ C-H2-F2-O3-S ]
37924-13-3 - perfluidone [C14H12F3NO4S2]
35367-38-5 - diflubenzuron [C14H9ClF2N2O2]
33245-39-5 - fluchloralin [C12H13ClF3N3O4]
31251-03-3 - fluotrimazole [C22H16F3N3]
29091-21-2 - prodiamine [C13H17F3N4O4]
29091-05-2 - dinitramine [C11H13F3N4O4]
28606-06-6 - na
28523-86-6 - Sevoflurane [ C4-H3-F7-O
]
27314-13-2 - norflurazon [C12H9ClF3N3O]
26675-46-7 - Isoflurane [ C3-H2-Cl-F5-O
]
26399-36-0 - profluralin [C14H16F3N3O4]
25366-23-8 - thiazafluron [C6H7F3N4OS]
24751-69-7 - Nucleocidin [ C10-H13-F-N6-O6-S
]
14477-72-6 - Acetic acid, trifluoro-, ion(1-) [ C2-F3-O2
]
9002-84-0 - Polytetrafluoroethylene (Teflon) ( (C2-F4)mult-
or (C2-F4)x-)
2837-89-0 - 1,1,1,2-Tetrafluoro-2-chloroethane (Freon 124) [
C2-H-Cl-F4 ]
2164-17-2 - fluometuron [C10H11F3N2O]
1861-40-1 - benfluralin [C13H16F3N3O4]
1827-97-0 - 2,2,2-Trifluoroethanesulfonic
acid [ C2-H3-F3-O3-S ]
1763-23-1 - Perfluorooctane sulfonic acid [ C8-H-F17-O3-S
]
1717-00-6 - 1,1-Dichloro-1-fluoroethane [ C2-H3-Cl2-F
]
1582-09-8 - trifluralin [C13H16F3N3O4]
1493-13-6 - Trifluoromethanesulfonic acid
[ C-H-F3-O3-S ]
811-97-2 - 1,1,1,2-Tetrafluoroethane (Norflurane) [ C2-H2-F4
]
754-91-6 - Perfluorooctanesulfonamide [ C8-H2-F17-N-O2-S
]
640-19-7 - fluoroacetamide [C2H4FNO]
513-62-2 - Fluoroacetate [ C2-H2-F-O2
]
453-13-4 - 1,3-Difluoro-2-propanol [
C3-H6-F2-O ]
420-46-2 - 1,1,1-Trifluoroethane [ C2-H3-F3
]
406-90-6 - Fluroxene (Ethene, (2,2,2-trifluoroethoxy)-) [ C4-H5-F3-O
]
370-50-3 - flucofuron [C15H8Cl2F6N2O]
335-76-2 - Perfluorodecanoic acid [ C10-H-F19-O2
]
335-67-1 - Perfluorooctanoic acid (PFOA) [ C8-H-F15-O2
]
311-89-7 - Perfluorotributylamine [ C12-F27-N
]
306-83-2 - 2,2-Dichloro-1,1,1-trifluoroethane [Freon 123) [
C2-H-Cl2-F3 ]
151-67-7 - 2-Bromo-2-chloro-1,1,1-trifluoroethane (HALOTHANE)
[ C2-H-Br-Cl-F3 ]
144-49-0 - Fluoroacetic acid [ C2-H3-F-O2
]
116-14-3 - Tetrafluoroethylene [ C2-F4
]
98-56-6 - 1-Chloro-4-(trifluoromethyl)benzene [ C7-H4-Cl-F3
]
88-30-2 - TFM (3-Trifluoromethyl-4-nitrophenol)[ C7-H4-F3-N-O3
]
79-38-9 - Chlorotrifluoroethylene [ C2-Cl-F3
]
76-38-0 - Methoxyflurane [ C3-H4-Cl2-F2-O
]
76-15-3 - Chloropentafluoroethane (Freon 115 )[C2-Cl-F5
]
76-14-2 - Dichlorotetrafluoroethane (Freon 114 )[ C2-Cl2-F4
]
76-13-1 - 1,1,2-Trichloro-1,2,2-trifluoroethane (Freon 113 )
[C2-Cl3-F3 ]
76-05-1 - Trifluoroacetic acid [ C2-H-F3-O2]
75-71-8 - Dichlorodifluoromethane (Freon 12) [ C-Cl2-F2]
75-69-4 - Trichloromonofluoromethane (
Freon 11, 11A, 11B) [C-Cl3-F]
75-68-3 - 1-Chloro-1,1-difluoroethane (Freon 142, Freon 142b)
[ C2-H3-Cl-F2]
75-45-6 - Chlorodifluoromethane (Freon 21) [ C-H-Cl-F2]
75-43-4 - Dichlorofluoromethane (Freon
21) [C-H-Cl2-F]
Gliftor
(70% 1,3-difluoro-2-propanol (DFP); 30% 1-chloro-3-fluoro-2-propanol)
is extensively used throughout both Russia and China for rodent
control (Feldwick et al. 1994).
Administration of the major ingredient of gliftor (DFP) to rats
generates signs typical of 1080 poisoning
(Mead et al. 1991). Although not tested on a wide
range of species, gliftor is expected to display target specificities
related to those of 1080 (Feldwick et al. 1994). It is
relatively non-toxic to birds (Fil'kenshtein et al. 1964; Golovanova
1970, 1972, both cited Feldwick et al. 1994.). Gliftor
has an advantage over 1080 in that 4-methylpyrazole has potential
to serve as an antidote if administered during the characteristic
2h lag phase (Feldwick et al. 1994).
Ref: Impact of 1080 on non-target species
and priorities for research. A report to the Browsing Animal
Research Council; by H L Statham. February 1996
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]
[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)
From Toxline at Toxnet
NEW ZEALAND JOURNAL OF ZOOLOGY; 20 (4). 1993.
329-334.
Sodium monofluoroacetate and alternative
toxins for possum control.
EASON CT, FRAMPTON CM, HENDERSON R, THOMAS
MD, MORGAN DR
Manaaki Whenua-Landcare Res., P.O. Box 31 011, Christchurch,
NEZ.
Sodium monofluoroacetate (1080) is still an essential tool
for possum control. We have reassessed the fate of this compound
in the environment, and found no evidence of water contamination
after large-scale possum control operations. The toxin is biodegradable
in all living systems and will not accumulate in the food chain.
Nevertheless, overreliance on a single toxin for a particular
pest, such as 1080 for possum control, is unwise, and we are
evaluating alternatives. Possums are susceptible
to some non-anticoagulant toxins, including gliftor,
cholecalciferol, calciferol, and alpha-chloralose. Of the anticoagulant
toxins, brodifacoum is more effective than pindone. Integrated
pen and field trials will determine the most cost-effective
alternatives to 1080 for use in bait stations and for aerial
application. Any alternative toxin will need to be subjected
to the same scrutiny as 1080 for its environmental fate and
impact on non-target species.
CAS Registry Numbers:
56073-10-0
56073-10-0
15879-93-3
8065-71-2
83-26-1
67-97-0
62-74-8
50-14-6
From Toxline at Toxnet
POCHVOZN AGROKHIM RASTIT ZASHT; 22 (1). 1987.
116-121.
Language: Bulgarian
IMPROVED CONTROL OF
MICROTUS-ARVALIS PALL
DEKOV O
BIOSIS COPYRIGHT: BIOL ABS. RRM PESTICIDES DIFENACOUM BROMADIOLONE
CHLOROPHACINONE CRIMIDINE GLIFTOR
CAS Registry Numbers:
56073-07-5
56073-07-5
28772-56-7
8065-71-2
3691-35-8
535-89-7
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3961873
Sud Med Ekspert. 1986 Jan-Mar;29(1):55-6.
[Gliftor poisoning]
[Article in Russian]
Buklan AI, Kravets AF.
Publication Types:
• Case Reports
PMID: 3961873 [PubMed - indexed for MEDLINE]
From Toxline at Toxnet
Khim. Sel'sk. Khoz. 15(11): 44-49 1977
(42 References)
Side-effects of pesticides on terrestrial
and aquatic zoocenoses.
Voronova LD
Cent. Lab. Environ. Prot., USSR Minist. Agric., USSR
PESTAB. Recent studies carried out in the USSR on the effects
of pesticides on the terrestrial and aquatic fauna are presented.
Massive deaths were observed in the wild fauna due to acute
poisoning with rat poisons, mercurials, arsenicals, organochlorine
pesticides, and 2,4-D butyl ester. The study of the environmental
distribution and persistence of carbaryl revealed the presence
of this pesticide in all components of the flora and fauna,
its accumulation along the trophic chains, as well as a reduction
of the populations of small rodents, hares and moles in the
biocenoses investigated. The application of 2,4-D butyl ester
in a single dose of 3.5-7 kg/ha in forests led to the reduction
of the entire population and of the percentage of young animals
in warm-blooded and cold-blooded zoocenoses. All components
of the biocenosis contained 2,4-D butyl ester and its metabolites
after the treatment. Experiments with
breasts of prey fed small rodents poisoned with the rat poison
gliftor showed general poisoning symptoms and occasional death.
Field experiments revealed long-term changes in the soil
fauna under the effect of carbamates, and only short-term effect
of organophosphorus pesticides.
CAS Registry Numbers:
63-25-2
63-25-2
94-75-7
8065-71-2
From Science Direct
Journal of Fluorine Chemistry; Volume 7, Issue 5 , May 1976,
Pages 537-539
Short Communication
Rotational isomerism in fluorinated
compounds: 1,3-difluoro-2-propanol
G. Crowder and Douglas Tennant
Department of Chemistry and Killgore Research Center West Texas
State University, Canyon, Texas 79016 U.S.A.
From Toxline at Toxnet
Gig. Tr. Prof. Zabol. (12): 53-54; 1975.
Three cases of gliftor poisoning.
Kovalenko LI, Bulkina VA, Panteleev RI
PESTAB. Acute poisoning with gliftor, a pesticide composed of
30% glycerol chlorofluorohydrin and 70% glycerol difluorohydrin,
was studied in three tractor drivers who, mistaking it for alcohol,
ingested 30 ml each of this liquid. Motor
disorders comprising complex chloreiform hyperkinesis (Kulenkampff-Tarnow
syndrome) due to lesions in the cortical and subcortical structures
of the corpus striatum and of the limbicoreticular portion of
the brain, were the principal poisoning symptoms. There
were no symptoms of fluorine poisoning. One patient,
who presented the first symptoms 48 hr after ingestion of the
poison, died in respiratory collapse 6 days later. Leukocytosis
(up to 20% rod neutrophilis) hyperglycemia, a serum potassium
level of 2.7 mEq/liter, proteinuria, pyuria, and hematuria were
observed. Histopathological examination
revealed acute circulatory disturbances in the internal organs,
parenchymatous dystrophy, and dystrophic changes in the central
nervous system.
CAS Registry Numbers: 8065-71-2
From Dart Special at Toxnet
ZAP LENINGR S KH INST 212:91-93,1973
EFFECT OF SUBLETHAL DOSES OF GLIFTOR
ON REPRODUCTION OF WHITE MICE
TATTAR AV
Taxonomic Name: MUS, WHITE
Test Object: MAMMAL, MOUSE
Name of Agent (CAS RN): GLIFTOR ( 8065-71-2
)
Assay Method: VIABILITY, FERTILITY AND MORTALITY
Language: Russian
From Toxline at Toxnet
TR INST KRAEV PATOL AKAD NAUK KAZ SSR; 22 1971
28-30
Morphological changes of internal organs
of experimental animals after oral administration of gliftor.
KNYSH VS, TKACH NZ, TSAREVSKII LP
The single administration of gliftor
(I; internally, 40-160 mg/kg) caused considerable destructive
changes and circulatory disorders in the internal organs of
rats. The maximum tolerance dose of I (60 mg/kg) caused hyperplasia
of the cells of the RES in the spleen, proliferation of local
cells, and inflammatory cellular infiltration of the alveolar
walls in the lungs.
CAS Registry Numbers:
453-13-4 - 1,3-Difluoro-2-propanol
453-11-2 - 2-Propanol, 1-chloro-3-fluoro-
From Toxline at Toxnet
TR INST KRAEV PATOL AKAD NAUK KAZ SSR; 22 1971
12-16
Change of the morphological composition
of the peripheral blood in gliftor poisoning.
TKACH NZ, MILOVANOVA VI, KNYSH VS
Rats were subjected to chronic inhalation of gliftor (I; 110,
64, 13, and 1 mg/m-3). A dose of 110 mg/m-3 beginning with the
30th day of poisoning caused pronounced
leukocytosis (maximum on the 72nd day), eosinophilia, and lymphopenia.
The contents of Hb, erythrocytes, and monocytes were close to
the control values. A dose of 64 mg/m-3 caused less leukocytosis
and insignificant changes of the content of neutrophils and
lymphocytes. With a dose of 1 mg/m-3 there
was a significant increase of the relative number of eosinophils
and decrease of the number of lymphocytes. This dose
was considered the threshold. With single cutaneous applications
the LD5- for rabbits was 66 plus or minus 10 mg/kg. The recommended
maximum allowable concentration of I for worker exposure in
the air of production rooms in 0.05 mg/m-3 (1/20 of the threshold
value).
CAS Registry Numbers:
453-13-4 - 1,3-Difluoro-2-propanol
453-11-2 - 2-Propanol, 1-chloro-3-fluoro-
From Toxline at Toxnet
TR INST KRAEV PATOL AKAD NAUK KAZ SSR; 22 1971
5-12
Effect of gliftor on certain metabolic
processes of experimental animals under inhalation poisoning
conditions.
TKACH NZ, KNYSH VS, MILOVANOVA VI, SHISHKOVA NK, SLEPOVA LI
Under conditions of the acute inhalation effect of the vapors
of gliftor (I) the LD50 for rats was 580 plus or minus 65 and
for mice 1260 plus or minus 15 mg/m-3. The threshold concentration
(TC) for rats with respect to brief disturbance of the functional
state of the CNS was 50 and the subthreshold 10 mg/m-3; for
mice the TC was 190 mg/m-3. Chronic (4
mo.) inhalation by rats of I in a concentration of 110 and 64
mg/m-3 disturbed the functional state of the CNS and antitoxic
and protein-forming functions of the liver and reduced oxidation-reduction
processes. I in a concentration of 1.0 mg/m-3 increased the
concent of eosinophils and reduced the number of lymphocytes
by the end of the poisoning period. I is a hazardous
compound. A maximum allowable concentration of I of 0.05 mg/m-3
in the air of production shops is recommended for worker exposure.
CAS Registry Numbers:
453-13-4 - 1,3-Difluoro-2-propanol
453-11-2 - 2-Propanol, 1-chloro-3-fluoro-
From Toxline at Toxnet
TR INST KRAEV PATOL AKAD NAUK KAZ SSR; 22 1971
23-28
Pathomorphological changes in internal
organs of white rats under the inhalation effect of gliftor.
KNYSH VS, TKACH NZ, TSAREVSKII LP, MILOVANOVA
VI
Rats were subjected to the single inhalation effect of vapors
of the zoocide gliftor (I; 50, 100, 350, 520, and 1100 mg/m-3).
Morphological changes were noted beginning with a concentration
of 350 mg/m-3. In a chronic experiment (4 mo.) the rats were
subjected to I poisoning in a concentration of 10, 13, 64, and
110 mg/m-3. Distinct morphological changes in the organs were
noted under the effect of concentrations 64 and 110 mg/m-3.
Under the chronic effect of I there were
considerable circulatory disorders and destructive changes of
the interanl organs, especially in the liver, lungs, spleen,
and kidneys.
CAS Registry Numbers:
453-13-4 - 1,3-Difluoro-2-propanol
453-11-2 - 2-Propanol, 1-chloro-3-fluoro-
From Toxline at Toxnet
TR INST KRAEV PATOL AKAD NAUK KAZ SSR; 22 1971
17-23
Effect of gliftor on rabbits under conditions
of chronic oral poisoning.
ALIEV KA, TKACH NZ, SHISHKOVA NK, KOLOD'KO
TP
The threshold concentration with respect to the effect of gliftor
(I) on the organoleptic properties of water is at the 1 mg/l
level. I has feeble cumulative properties. Rabbits tolerated
the chronic oral administration with water of 1/10 and 1/20
LD50 of I, receiving in all 11.2-5.6 LD50. In this case leukocytosis,
an increase of the quantity of coproporphyrin
excreted in the urine, and an increase
of the blood nucleic acid level were noted. The threshold
dose is close to 0.15 mg/mg (3.0 mg/l). The organoleptic sign
is the limiting factor in establishing the maximum allowable
concentration of I in water.
CAS Registry Numbers:
453-13-4 - 1,3-Difluoro-2-propanol
453-11-2 - 2-Propanol, 1-chloro-3-fluoro-
From Toxline at Toxnet
Byull. Vses. Nauch-Issled. Inst. Zashch. R; 7(2): 38-43; 1970
Language: Russian
Primary and secondary effects of the
rodenticide Gliftor in birds.
Golovanova EN
The effects of the rodenticide Gliftor (difluorohydrine of glycerine
plus chlorofluorohydrine of glycerine) were studied on birds.
Feeding tests revealed the slow development of a repellent effect
of Gliftor mixed with bait in proportions up to 10%. The lethal
doses, determined for 14 different species such as goose, wild
duck, teal, black kite, windhover, sparrow, chicken, pigeon,
crow, rook, magpie, and blackbird, ranged from 500 to 3,000
mg/kg. Gliftor was found to be more toxic
in nestlings than in adult birds; no resistance or increased
sensitivity to the poison developed over time. Temporary loss
of weight was observed in nestlings 1-2 days following the ingestion
of sublethal doses. Egg production, fertility, or the development
of embryos and nestlings were not affected by sublethal doses.
The retention times in eggs and meat of chickens fed diets containing
1-10% Gliftor were three and five days, respectively. Cats
fed such eggs and meat died.
From Toxline at Toxnet
J REPROD FERT 21:263-266,1970
MALE ANTIFERTILITY COMPOUNDS: STRUCTURE
AND ACTIVITY RELATIONSHIPS OF U-5897, U-15,646 AND RELATED SUBSTANCES
ERICSSON RJ, YOUNGDALE GA
Taxonomic Name: RATTUS
Test Object: MAMMAL, RAT
Sex Treated: MALE
Name of Agent (CAS RN):
3-CHLORO-1,2-PROPANEDIOL ( 96-24-2 )
1,1'-(PENTAMETHYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL)
1-CHLORO-3-ISOPROPOXY-2-PROPANOL ( 4288-84-0 )
3-CHLORO-1,2-PROPANEDIOL-1-ACETATE ( 24573-30-6 )
1,1'-(PENTAMETHYLENEDIOXY)BIS(3-FLUORO-2-PROPANOL)
( 64508-93-6 )
1,1'-((1,4-CYCLOHEXYLENE)BIS(METHYLENEOXY))BIS(3-CHLORO-2-PROPANOL),TRANS
1,1'-(TRIMETHYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL)
5-(3-CHLORO-2-HYDROXYPROPOXY)-1-PENTANOL ( 18485-61-5 )
1,1'-(P-PHENYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL) ( 15129-28-9
)
1,1'-(HEXAMETHYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL) ( 20387-39-7
)
1,1'-(DECAMETHYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL) ( 24765-68-2
)
1,1'-(2-BUTYNYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL) ( 1606-83-3
)
1,1'-(PENTAMETHYLENEDIOXY)BIS(3-BROMO-2-PROPANOL) ( 64508-92-5
)
2-CHLOROETHANOL ( 107-07-3 )
1,1'-(ETHYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL) ( 13078-45-0 )
1-CHLORO-3-PHENOXY-2-PROPANOL ( 4769-73-7 )
3-CHLORO-1,2-PROPANEDIOL-1-BENZOATE ( 3477-94-9 )
1,1'-(OXYBIS(ETHYLENEOXY))BIS(3-CHLORO-2-PROPANOL) ( 45207-66-7
)
1,1'-(TETRAMETHYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL) ( 14180-03-1
)
1,1'-(1,4-CYCLOHEXYLENEBIS(METHYLENEOXY))BIS(3-CHLORO-2-PROPANOL),CIS
1,1'-(PROPYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL) ( 18371-82-9 )
1,1'-(3,3-DIMETHYLPENTAMETHYLENE)BIS(3-CHLORO-2-PROPANOL) (
64425 )
-92-9
1-CHLORO-3-(2-HYDROXYETHOXY)-2-PROPANOL ( 18371-74-9 )
1-CHLORO-3-FLUORO-2-PROPANOL ( 453-11-2
)
1,1'-(PENTAMETHYLENEDIOXY)BIS(3-IODO-2-PROPANOL) ( 64508-94-7
)
3-BROMO-1,2-PROPANEDIOL ( 4704-77-2 )
3,3,3-TRICHLORO-1,2-PROPANEDIOL ( 815-02-1 )
1,3-DICHLORO-2-PROPANOL ( 96-23-1 )
1-CHLORO-3-(PENTYLOXY)-2-PROPANOL ( 25401-93-8 )
1,1'-(PENTAMETHYLENEDIOXY)BIS(3-CHLORO-2-PROPANOL)DIACETATE
( 247 )
71-52-6
Assay Method:
REPRODUCTIVE TOXICITY
