From
Toxline at Toxnet
Toxicologist
1990 Feb;10(1):175
Subchronic
and reproductive toxicity and teratology of haloxyfop
herbicide.
Quast JF, Yano BL, Dietz FK, Marler
RM, Hayes WC
Toxicology Research Laboratory, The
Dow Chemical Company, Midland, MI.
The subchronic toxicity of haloxyfop (2-(4-((3-chloro-5-(trifluoromethyl)-2-
pyridinyl)oxy)phenoxy)propanoic acid) herbicide,
a peroxisome proliferator, was evaluated in rats, mice,
dogs and monkeys. Male rats given 0.2 or 2.0
mg/kg/day and female rats given 2.0 mg/kg/day in feed
for 16 weeks had peroxisome associated
hepatocellular hypertrophy. Male and female rats
given 2.0 mg/kg/day for 37 weeks also had increased
renal tubular pigment. Mice given 2.0 mg/kg/day
in feed for 13 weeks had peroxisome associated hepatocellular
hypertrophy. Dogs fed 20 mg/kg/day and monkeys gavaged
with 30 mg/kg/day for 13 weeks had hepatocellular
hypertrophy, decreased size of thyroid follicles, and
decreased red blood cell counts and serum cholesterol.
Hepatocellular effects in dogs and monkeys were not
associated with peroxisome proliferation. No-observed
effect levels were between 0.02 and 0.2 mg/kg/day for
rats, 0.2 mg/kg/day for mice, and 2 mg/kg/day for dogs
and monkeys. There were no effects on reproduction in
rats at dose levels up to 1.0 mg/kg/day or evidence
of teratogenicity in rats or rabbits at dose levels
up to 7.5 or 20 mg/kg/day, respectively.
CAS
Registry Number: Haloxyfop
(69806-34-4)
|
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8566486&dopt=Abstract
Fundam
Appl Toxicol 1995 Nov;28(1):71-9
Species-dependent
induction of peroxisome proliferation by haloxyfop,
an aryloxyphenoxy herbicide.
Stott WT, Yano BL, Williams DM,
Barnard SD, Hannah MA, Cieszlak FS, Herman JR.
Dow Chemical Company, Midland,
Michigan 48674, USA.
The potential of haloxyfop [2-(4-((3-chloro-5-(trifluoromethyl)-2-
pyridinyl)oxy)phenoxy)propanoic acid; HAL] to induce
the proliferation of hepatocellular
peroxisomes (PP) was examined in rats, mice,
dogs, and monkeys. Chemically induced PP is associated
with the development of liver tumors in rodents via
an apparent species-dependent, nongenotoxic mechanism
of action. HAL is nongenotoxic yet has been shown to
cause liver tumors in female B6C3F1 mice.
Ingestion of HAL by rats and/or mice (0.1-14 mg/kg/day
for 2 to 4 weeks) resulted in significant dose-related
PP as evidenced by hepatocellular hypertrophy, increased
peroxisome volume density (VD), and induction of peroxisomal
enzymes and CYP4A1. Only a relatively weak induction
of PP was noted at a carcinogenic dosage in female mice.
In contrast to rodent species, ingestion of up to 20
mg/kg/day HAL by male and female Beagle dogs for 13
weeks failed to increase peroxisomal VD while causing
only a slight increase in peroxisomal enzyme activity
at the highest dosages. Oral administration of up to
30 mg/kg/day HAL by male and female Cynomolgus monkeys
for 13 weeks failed to induce PP. While
a direct relationship of PP with tumor formation, at
least in mice, was not demonstrated, these data still
support the concept that PP represents a potential marker
of nongenotoxic tumorigenic activity, at some dosage,
in rodents.
PMID: 8566486 [PubMed - indexed for
MEDLINE]
|
From
Toxline at Toxnet
Bulletin
of Environmental Contamination and Toxicology, Vol.
51, No. 4, pages 625-632, 15 references, 1993
Developmental
Toxicity of Haloxyfop Ethoxyethyl
Ester in the Rat
Machera K
The developmental toxicity of haloxyfop-ethoxyethyl-ester
(87237-48-7) (HEE) was studied in rats. Pregnant
Wistar-rats were gavaged with 5, 10, or 50mg/kg HEE
on days six to 16 of gestation. They were observed for
clinical signs of toxicity and sacrificed on gestational
day 21. The uteri were removed, examined, and the number
of implantations, live and dead fetuses, and resorption
sites recorded. The live fetuses were weighed and examined
for malformations. HEE at 10 and 50mg/kg caused vaginal
bleeding in 40 and 50% of the dams, respectively. The
10 and 50mg/kg doses significantly increased
the number of resorptions per litter and decreased the
number of live fetuses per litter. The 50mg/kg
dose caused a significant decrease
in fetal weight. HEE caused
a significant dose related increase in the number of
cachectic fetuses. The
proportion of cachectic fetuses following exposure to
5, 10, and 50mg/kg was 2.0, 6.8, and 20.3%, respectively.
Ureterohydronephrosis was
the most frequently observed soft tissue malformation,
the prevalence of this defect following the 10 and 50mg/kg
doses being 42.9 and 54.8%, respectively. The 10 and
50mg/kg doses caused skeletal
malformations such as retarded ossification of the sternum
and absence of rib 13. The author concludes
that haloxyfop-ethoxyethyl-ester is embryotoxic and
teratogenic. The no observable effect
level is expected to be below 5mg/kg.
|
From
Toxline at Toxnet
Pesticide
residues in food - 1995.
Toxicology evaluations (1996) pp 203-29
Haloxyfop
FAO and WHO working groups
Levels that cause no toxic effect.
Mouse:
0.03 mg/kg bw per day (two-year study of toxicity and
carcinogenicity).
Rat:
0.065 mg/kg bw per day (two-year study of toxicity and
carcinogenicity and study of reproductive toxicity);
1 mg/kg bw per day (maternal, embryo-, and fetotoxicity
in study of developmental toxicity).
Rabbit:
7.5 mg/kg bw per day (maternal toxicity in study of
developmental toxicity).
Dog:
0.5 mg/kg bw per day (12-month study of toxicity).
Monkey:
2 mg/kg bw per day (13-week study of toxicity).
Humans:
Estimate of acceptable daily intake 0-0.0003 mg/kg bw.
CAS
Registry Number: 69806-34-4
|
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15079078
Proc Natl Acad Sci U S A. 2004
Apr 20;101(16):5910-5. Epub 2004 Apr 12.
Molecular basis for the inhibition of
the carboxyltransferase domain of acetyl-coenzyme-A carboxylase
by haloxyfop and diclofop.
Zhang H, Tweel B, Tong L.
Department of Biological Sciences, Columbia University, New
York, NY 10027, USA.
Acetyl-CoA carboxylases (ACCs) are crucial for the metabolism
of fatty acids, making these enzymes important targets for the
development of therapeutics against obesity, diabetes, and other
diseases. The carboxyltransferase (CT) domain of ACC is the
site of action of commercial herbicides, such as haloxyfop,
diclofop, and sethoxydim. We have determined the crystal structures
at up to 2.5-A resolution of the CT domain of yeast ACC in complex
with the herbicide haloxyfop or diclofop. The inhibitors are
bound in the active site, at the interface of the dimer of the
CT domain. Unexpectedly, inhibitor binding requires large conformational
changes for several residues in this interface, which create
a highly conserved hydrophobic pocket that extends deeply into
the core of the dimer. Two residues that affect herbicide sensitivity
are located in this binding site, and mutation of these residues
disrupts the structure of the domain. Other residues in the
binding site are strictly conserved among the CT domains.
PMID: 15079078 [PubMed - indexed for MEDLINE]
From Toxline at Toxnet
Document Numbers:
CRISP/98/ES07929-01A1
CRISP/99/ES07929-02
CRISP/1999/ES07929-03
CRISP/2000/ES07929-04
CRISP/2001/ES07929-05
Source: Crisp Data Base National Institutes of Health
Supporting Agency: U.S. DEPT. OF HEALTH AND HUMAN SERVICES;
PUBLIC HEALTH SERVICE; NATIONAL INSTITUTES OF HEALTH, NATIONAL
INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES
2001 - CHEMICAL
EFFECTS ON METABOLISM AND REPRODUCTION
HAASCH ML
MLHAASCH@OLEMISS.EDU, UNIVERSITY OF MISSISSIPPI, 347 FASER
HALL, P.O. BOX 1848, UNIVERSITY, MS 38677-1848
DESCRIPTION (Adapted from the APPLICANT'S ABSTRACT): The broad,
long-term goals of the proposed research are to understand the
mechanism(s) by which peroxisome proliferating agents (PPAs)
interfere with signaling cross-talk between metabolic pathways
and nuclear hormone receptors producing perturbations in reproduction
and development. PPAs are a structurally-diverse group of chemicals
including herbicides, solvents, and plasticizers, that are known
fatty acid, retinoid and endocrine disrupters. These metabolic
pathways interact in the regulation of gene expression for reproduction
and development. Hepatic peroxisome proliferation by PPAs has
species-specificity (rats are sensitive, humans are not) but
little is known about the mechanisms of PPAs endocrine disruptive
effects. PPA species-specificity has recently been demonstrated
in fish allowing investigation of responsive and non-responsive
models. Fish exposed to PPAs can bioaccumulate these xenobiotics,
and serve as biomarkers of exposure and effect. Furthermore,
because human consumption of fish and fish products has increased
in the last decade, it is imperative that we understand the
potential for adverse effects by these contaminants. Test organisms
will be a commercially-important food species, the catfish (sensitive;
Haasch, 1996), and a model species, the Japanese medaka (non-sensitive;
Scarano et al,. 1994). The proposed research
will test the hypothesis that PPAs are endocrine disrupters
producing perturbations in reproduction and development. PPAs
to be investigated are: clofibrate, as a model PPA, and
haloxyfop enthoxyethyl, di-n-butyl-ortho-phthalate
(DBoP) and tetrachloroethylene (PCE) as environmental contaminant
PPAs. Specific Aims include, 1) determining if PPA-sensitivity
is ruired for endocrine disruption and if PAPAS from different
chemical classes cause endocrine disruption by similar mechanisms,
2) determination of specific mechanisms of endocrine disruption
by examining PPA combinations, and 3) determining if PPA-mediated
endocrine disruption can be correlated with reproductive or
developmental problems and if PPA exposure produces metabolic
alterations in offspring. The proposed investigation will provide
insight into cell signaling cross-talk between metabolic pathways
and nuclear hormone receptors, endocrine disruption, and the
developmental and reproductive effects of PAPAS.
From Toxline at Toxnet
VOPROSY ONKOLOGII (ST. PETERSBURG); 44 (4). 1998.
468-476.
Once again about the issue of threshold
in chemical carcinogenesis.
TURUSOV VS, RAKITSKY VN, REVAZOVA YU A
BIOSIS COPYRIGHT: BIOL ABS. RRM JOURNAL ARTICLE MOUSE RAT HUMAN
ANIMAL MODEL PATIENT ONCOLOGY TOXICOLOGY CHEMICAL CARCINOGENESIS
GENOTOXICITY GENOTOXIC CARCINOGENS EPIGENETIC CARCINOGENS PHENOBARBITAL
PEROXISOME PROLIFERATION STIMULANTS SACCHARINE D-LIMONENE SPONTANEOUS
INITIATION CYTOTOXICITY APOPTOSIS OXIDATIVE STRESS RISK EVALUATION
THRESHOLD PROBLEM
Keywords:
Cytology and Cytochemistry-Animal
Cytology and Cytochemistry-Human
Genetics and Cytogenetics-Animal
Genetics and Cytogenetics-Human
Biochemical Studies-General
Toxicology-General
Neoplasms and Neoplastic Agents-General
Hominidae
Muridae
CAS Registry Numbers:
52214-84-3 - Ciprofibrate
69806-34-4 - Haloxyfop
49562-28-9 - Fenofibrate
76-44-8 - Heptachlor
5989-27-5 - (D)-Limonene
10540-29-1 - Tamoxifen
103-23-1 - Dioctyl adipate
637-07-0 - Clofibrate
110-00-9 - Furan
309-00-2 - Aldrin
123-91-1 - 1,4-Dioxane
84-74-2 - Dibutyl phthalate
81-07-2 - Saccharin
60-57-1 - Dieldrin
57-97-6 - 9,10-Dimethyl-1,2-benzanthracene
57-74-9 - Chlordane
50-29-3 - DDT
50-06-6 - Phenobarbital
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]
From Toxline at Toxnet
Source: HABERER, K. (ED.). VOM WASSER, BAND 86; (WATER, VOL.
86). XV+455P. VCH VERLAGSGESELLSCHAFT MBH: WEINHEIM, GERMANY;
VCH PUBLISHERS, INC.: NEW YORK, NEW YORK, USA. ISBN 3-527-28679-9.;
86 (0). 1996. 247-262.
SEWAGE WORKS AS THE MAIN SOURCE OF PESTICIDES
IN SURFACE WATER-BALANCE OF THE ENTRY
SEEL P, KNEPPER TP, GABRIEL S, WEBER A,
HABERER K
Abstract:
BIOSIS COPYRIGHT: BIOL ABS. RRM BOOK CHAPTER SEWAGE WORKS PESTICIDE
PESTICIDES SEWAGE DRAIN SAMPLING RAIN PUDDLE ANALYSIS POLLUTION
ASSESSMENT CONTROL AND MANAGEMENT FIELD METHOD ANALYTICAL METHOD
RIVER MAIN GERMANY
CAS Registry Numbers: [too many to list]
69806-34-4
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1347398&dopt=Abstract
Life Sci
1992;50(7):533-40
Coenzyme
A esters of 2-aryloxyphenoxypropionate herbicides and 2-arylpropionate
antiinflammatory drugs are potent and stereoselective inhibitors
of rat liver acetyl-CoA carboxylase.
Kemal C, Casida JE.
Department of Entomological Sciences, University of California,
Berkeley 94720.
The CoA esters of diclofop, haloxyfop
and fluazifop are up to 425-fold more potent than the corresponding
unconjugated herbicides as inhibitors of rat liver acetyl-CoA
carboxylase (EC 6.4.1.2); the most potent inhibitor is (R)-fluazifopyl-CoA2
(Ki = 0.03 microM). The binding site is stereoselective
for (R)-diclofop, the herbicidally active enantiomer, and for
(R)-diclofopyl-CoA. The CoA esters of the antiinflammatory drugs
ibuprofen and fenoprofen also strongly inhibit this carboxylase.
(S)-Ibuprofenyl-CoA (Ki = 0.7 microM), the CoA ester of the
enantiomer with antiinflammatory activity, is 15-fold more potent
as an inhibitor than (R)-ibuprofenyl-CoA. These results suggest
that some of the biological effects of these herbicides and
antiinflammatory drugs in animals may be due to the inhibition
of acetyl-CoA carboxylase by their acyl-CoA derivatives.
PMID: 1347398 [PubMed - indexed for MEDLINE]
From Toxline at Toxnet
ENVIRON MANAGE; 16 (1). 1992.
21-32. [BIOSIS]
GERMAN DRINKING WATER REGULATIONS PESTICIDES
AND AXIOM OF CONCERN
DIETER HH
CAS Registry Numbers: [too many to list]
69806-34-4
From Toxline at Toxnet
ENVIRON INT; 16 (3). 1990. 219-230.
Bioconcentration of haloxyfop-methyl
in bluegill (Lepomis macrochirus Rafinesque).
MURPHY PG, LUTENSKE NE
Health and Environmental Sci., Dow Chem.
Comp., Midland, Mich. 48674, USA.
BIOSIS COPYRIGHT: BIOL ABS. Bluegill (Lepomis macrochirus Rafineseque)
were exposed to a 14C haloxyfop-methyl (methyl 2-(4-((3-chloro-5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoate)
concentration averaging 0.29 mug under flow-through conditions
for 28 days. At the end of 28 days, the fish were transferred
to clean water for a 4-day flow-through clearance period. Bluegill
were found to rapidly absorb the ester from water which was
then biotransformed at an extremely fast rate within the fish,
such that essentially no haloxyfop-methyl was detected in the
fish. The estimated bioconcentration factor for haloxyfop-methyl
in whole fish was < 17, based upon the detection limit for
the ester in fish (0.005 mug/g) and the average concentration
of haloxyfop-methyl in exposure water (0.29 mug/L). The
principal component of the 14C residue within whole fish was
haloxyfop acid (2-(4-((3-chloro-5-(trifluoromethyl)-2-pyridinyl)oxy)phenoxy)propanoic
acid) which accounted for an average of about 60% of
t [abstract truncated]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=2568910
Drug Metab Dispos. 1989 May-Jun;17(3):286-91.
Stereochemical inversion of haloxyfop
in the Fischer 344 rat.
Bartels MJ, Smith FA.
Analytical and Environmental Chemistry, Health and Environmental
Sciences, Dow Chemical Company,
Midland, MI 48674.
The 2-aryloxypropionate haloxyfop is currently being evaluated
for use as a herbicide. This compound is structurally similar
to a group of 2-arylpropionates that have been shown previously
to undergo stereochemical inversion in a variety of mammalian
species. To support the data obtained from a number of toxicity/oncongenicity
studies, in which racemic haloxyfop was employed, the stereochemical
disposition of this compound was examined in the Fischer 344
rat. After administration of racemic haloxyfop (11 mg/kg, po)
to male and female Fischer 344 rats, the day 1-10 urine samples
were fortified with D4-haloxyfop (center ring label) and extracted,
and the haloxyfop enantiomers were converted to diastereomeric
derivatives [(S)-phenylethylamine] and analyzed by gas chromatography-mass
spectrometry (GC/MS). Fecal samples for days 1-10 were fortified
with D4-haloxyfop, extracted, and purified by reverse phase
high-pressure liquid chromatography prior to derivation and
GC/MS analysis. In the female rat, 77.3% of the administered
dose was recovered in the day 1-10 urine and feces as parent
compound. The stereochemistry of the haloxyfop
present in these samples was found to be nearly all (R)-enantiomer
(greater than 98%). In the male rat, 52.2% of the dose
was recovered in the day 1-10 urine and feces as haloxyfop.
The stereochemistry of the parent compound present in these
samples was similar to the results seen in the female rat [greater
than 98% (R)]. These results show that
(S)-haloxyfop undergoes rapid and nearly complete inversion
to the (R)-enantiomer in the female Fischer 344 rat. The data
also suggest a similar stereochemical inversion of haloxyfop
in the male Fischer 344 rat.
PMID: 2568910 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3690005&dopt=Abstract
Bull Environ
Contam Toxicol 1987 Nov;39(5):797-801
Persistence
studies
with the herbicide, haloxyfop-methyl, in prairie field plots.
Smith AE.
Agriculture Canada, Research Station, Regina, Saskatchewan.
PMID: 3690005 [PubMed - indexed for MEDLINE]
From Toxline at Toxnet
WEED SCI; 34 (1). 1986. 81-87.
THE EFFECT OF ADJUVANTS AND OIL CARRIERS
ON PHOTODECOMPOSITION OF 2 4-D BENTAZON AND HALOXYFOP
HARRISON SK, WAX LM
BIOSIS COPYRIGHT: BIOL ABS. RRM PETROLEUM OIL CONCENTRATE SOYBEAN
OIL CONCENTRATE EMULSIFIER PACKAGE OXYSORBIC PHYTOTOXICITY UV
CAS Registry Numbers:
69806-34-4 - Haloxyfop
25057-89-0 - Bentazone
94-75-7 - 2,4-D
