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Order
No. |
Title |
Abstract
/ Keywords |
NTIS/PB88-245931
861p |
1988
- Health Advisories for 50 Pesticides (Including Acifluorfen,
Ametryn, Ammonium Sulfamate, Atrazine, Baygon, Bentazon, Bromacil,
Butylate, Carbaryl, Carboxin, Chloramben, Chlorothalonil,
Cyanazine, Dalapon, Dacthal, Diazinon, Dicamba, 1,3-Dichloropropene,
Dieldrin, Dimethrin, Dinoseb, Diphenamid, Disu
Environmental
Protection Agency, Washington, DC. Office of Drinking Water.
|
The documents
summarize the health effects of 50 pesticides including: acifluorfen,
ametryn, ammonium sulfamate, atrazine, baygon, bentazon, bromacil,
butylate, carbaryl, carboxin, chloramben, chlorothalonil, cyanazine,
dalapon, dacthal, diazinon, dicamba, 1,3-dichloropropene, dieldrin,
dimethrin, dinoseb, diphenamid, disulfoton, diuron, endothall,
ethylene thiourea, fenamiphos, fluometuron, fonofos, glyphosate,
hexazinone, maleic hydrazide, MCPA, methomyl, methyl parathion,
metalachlor, metribuzin, paraquat, picloram, prometon, pronamid,
propachlor, propazine, propham, simazine, 2,4,5-T, tebuthiuron,
terbacil, terbufos, and trifluralin. Topics discussed include:
General Information and Properties, Pharmokinetics, Health Effects
in Humans and Animals, Quantification of Toxicological Effects,
Other Criteria and Standards, Analytical Methods, and Treatment
Technologies. Supersedes PB88-113543. |
NTIS/PB88-113543
820p |
1987
-
Health Advisories for 50 Pesticides (Including Acifluorfen,
Ametryn, Ammonium Sulfamate, Atrazine, Baygon, Bentazon, Bromacil,
Butylate, Carbaryl, Carboxin, Chloramben, Chlorothalonil,
Cyanazine, Dalapon, Dacthal, Diazinon, Dicamba, 1,3-Dichloropropene,
Dieldrin, Dimethrin, Dinoseb, Diphenamid, Disu
Environmental
Protection Agency, Washington, DC. Office of Drinking Water.
|
These documents
summarize the health effects of 50 pesticides including: acifluorfen,
ametryn, ammonium sulfamate, atrazine, baygon, bentazon, bromacil,
butylate, carbaryl, carboxin, chloramben, chlorothalonil, cyanazine,
dalapon, dacthal, diazinon, dicamba, 1,3-dichloropropene, dieldrin,
dimethrin, dinoseb, diphenamid, disulfoton, diuron, endothall,
ethylene thiourea, fenamiphos, fluometuron, fonofos, glyphosate,
hexazinone, maleic hydrazide, MCPA, methomyl, methyl parathion,
metolachlor, metribuzin, paraquat, picloram, prometon, pronamid,
propachlor, propazine, propham, simazine, 2,4,5-T, tebuthiuron,
terbacil, terbufos, and trifluralin. Topics discussed include:
General Information and Properties, Pharmacokinetics, Health
Effects in Humans and Animals, Quantification of Toxicological
Effects, Other Criteria Guidance and Standards, Analytical Methods,
and Treatment Technologies. Draft rept. See also PB86-118338. |
NTIS/PB86-158219
24p |
1985
-
Analyses of Groundwater for Trace Levels of Pesticides,
Authors:
Lavy TL, Mattice JD, Cavalier TC
Arkansas
Water Resources Research Center, Fayetteville.
Arkansas Univ., Fayetteville. Dept. of Agronomy.
Prepared
in cooperation with Arkansas Univ.,
Fayetteville. Dept. of Agronomy. Sponsored by Geological Survey,
Reston, VA. Water Resources Div. |
Agricultural
production is a major source of revenue in Arkansas. In order
to increase productivity, it has been necessary to rely increasingly
on the use of pesticides and irrigation water. In the last 15
years several states have reported finding pesticides in groundwater
as a result of normal agricultural practices. Multiresidue analytical
techniques were developed for the analysis of acifluorfen,
alachlor, atrazine, cyanazine, diuron, fluormeturon, linuron,
metolachlor and propanil from groundwater. Analytical sensitivities
ranged from 1 to 10 ppb. The major objective of the study was
to collect groundwater samples from irrigation wells in areas
of southeastern Arkansas where pesticides are intensively used
and to analyze these samples for trace levels of pesticides
that are commonly used in these areas. |
NTIS/PB82-111857
67p |
1980
-
The Activity and Post-Emergency Selectivity of Some Recently
Developed Herbicides: R 40244, DPX 4189, Acifluorfen,
ARD 34/02 (NP 55) and PP 009
Authors:
Richardson WG, West TM, Parker C
Agricultural
Research Council, Oxford (England). Weed Research Organization.
|
The
present report gives indications of the post-emergence selectivity
of five new herbicides. Results of activity experiments are
also included for DPX 4189, ARD 34/02 (NP 55) and PP 009 to
provide information on levels of phytotoxicity, type and route
of action. Technical rept. Also pub. as ISSN-0511-4136.
[Blazer] |
NTIS/PB82-111931
82p |
1979
- The Activity and Pre-Emergence Selectivity of Some Recently
Developed Herbicides: R 40244, AC 206784, Pendimethalin, Butralin,
Acifluorfen and FMC 39821
Authors:
Richardson WG, West TM, Parker C
Agricultural Research Council, Oxford (England). Weed Research
Organization. |
The
present report gives pre-emergence selectivity data on R 40244,
AC 206784, pendimethalin, butralin, acifluorfen and FMC 39821.
Results of activity experiments are also included for five
of these to provide information on levels of phytotoxicity,
type and route of action. Technical rept. Also pub. as ISSN-0511-4236.
[Blazer] |
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12848506
J Agric Food Chem. 2003 Jul 16;51(15):4331-7.
Soil photolysis of herbicides in a moisture-
and temperature-controlled environment.
Graebing P, Frank MP, Chib JS.
Pittsburgh Environmental Research Laboratory, Inc., 3210 William
Pitt Way, Pittsburgh, Pennsylvania 15238, USA.
The problem of maintaining the moisture content of samples throughout
the course of a soil photolysis study is addressed. The photolytic
degradations of asulam, triclopyr, acifluorfen,
and atrazine were independently compared in air-dried soils and
in moist (75% field moisture capacity at 0.33 bar) soils maintained
at initial conditions through the use of a specially designed
soil photolysis apparatus. Each pesticide was applied at 5 microg/g.
The exposure phase extended from 144 to 360 h, depending on the
half-life of the compound. A dark control study, also using moist
and air-dried soils, was performed concurrently at 25 degrees
C. The results showed significant differences
in half-life. The dissipations generally demonstrated a
strong dependence on moisture. In most cases, photolytic degradation
on air-dried soil was longer than in the moist dark control soils.
Half-lives in dry soil were 2-7 times longer, and in the case
of atrazine, the absence of moisture precluded significant degradation.
Moist soil experiments also tended to correlate more strongly
with linear first-order degradations. The dark control experiments
also demonstrated shorter half-lives in moist soil. Moisture was
also observed to affect the amount of degradate formed in the
soils.
PMID: 12848506 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12758057&dopt=Abstract
Toxicol Appl
Pharmacol. 2003 May 15;189(1):28-38.
Experimental
hepatic uroporphyria induced by the diphenyl-ether herbicide fomesafen
in male DBA/2 mice.
Krijt
J, Psenak O, Vokurka M, Chlumska A, Fakan F.
Institute
of Pathophysiology, 1st Medical Faculty, Charles University, 128
53, Prague, Czech Republic
Hepatic uroporphyria
can be readily induced by a variety of treatments in mice of the
C57BL strains, whereas DBA/2 mice are almost completely resistant.
However, feeding of the protoporphyrinogen oxidase-inhibiting
herbicide fomesafen (0.25% in the diet for 18 weeks) induced hepatic
uroporphyria in male DBA/2N mice (liver porphyrin content up to
150 nmol/g, control animals 1 nmol/g), whereas fomesafen-treated
male C57BL/6N mice displayed only a slight elevation of liver
porphyrins ( approximately 5 nmol/g). The profile of accumulated
hepatic porphyrins in fomesafen-treated DBA/2N mice resembled
the well-characterised uroporphyria induced by polyhalogenated
aromatic hydrocarbons, while histological examination confirmed
the presence of uroporphyria-specific cytoplasmic inclusions in
the hepatocytes. Uroporphyrinogen decarboxylase activity decreased
to about 30% of control values in fomesafen-treated DBA/2N mice;
microsomal methoxyresorufin O-dealkylase activity was slightly
reduced. The amount of CYP1A1 and CYP1A2 mRNA, as determined by
real-time PCR, was not significantly changed; mRNA encoding the
housekeeping 5-aminolevulinic acid synthase was elevated 10-fold.
Total liver iron was slightly increased.
A similar uroporphyria was induced by the herbicide formulation
Blazer, containing a structurally related herbicide acifluorfen,
when fed to DBA/2N mice at a dose corresponding to 0.25% of acifluorfen
in the diet. Since DBA/2 mice are almost completely resistant
to all well-characterised porphyrogenic chemicals, the results
suggest the possible existence of a yet unknown mechanism of uroporphyria
induction, to which the DBA/2 mouse strain is more sensitive than
the C57BL strain.
PMID: 12758057
[PubMed - in process]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11837431&dopt=Abstract
J Environ
Qual. 2002 Jan-Feb;31(1):268-74.
Photochemistry
and photoinduced toxicity of acifluorfen, a diphenyl-ether herbicide.
Scrano
L, Bufo SA, D'Auria M, Meallier P, Behechti A, Shramm KW.
Dipartimento
di Produzione Vegetale, Universita della Basilicata, Potenza,
Italy.
Photochemistry studies
can be helpful in assessing the environmental fate of chemicals.
Photochemical reactions lead to the formation of by-products that
can exhibit different toxicological properties from the original
compound. For this reason the photochemical behavior of the herbicide
acifluorfen (5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoic
acid) in the presence of different solvents was studied. Photochemical
reactions were carried out using a high-pressure mercury arc and
a solar simulator. Kinetic parameters and quantum yields were
determined. The identification of photoproducts was performed
by mass spectrometry and [1H] nuclear magnetic resonance (NMR).
Nitrofluorfen, hydroxy-nitrofluorfen, 2-chloro-4-(trifluoromethyl)phenol,
5-trifluoromethyl-5'-nitrodibenzofuran, and other derivatives
were identified. The photochemical reactions were also carried
out in the presence of either a singlet or a triplet quencher,
and in the presence of either a radical initiator or a radical
inhibitor. Substances used as inhibitors of the excited levels
T1 and S1 showed that photodegradation of acifluorfen begins from
a singlet state S1 through a pi,pi* transition. The role of free
radicals in the photodegradation of acifluorfen was determined
and a radical mechanism was proposed. Toxicity
tests against Daphnia magna Strauss showed that acifluorfen was
not toxic at a concentration of 0.1 mM; however, photoproducts
formed after 36 h of UV exposure of the herbicide induced a remarkable
toxicity to the test organism.
PMID: 11837431
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11455817&dopt=Abstract
Pest Manag
Sci. 2001 Apr;57(4):372-9.
Photochemical
transformation of acifluorfen under laboratory and natural conditions.
Vialation
D, Baglio D, Paya-Perez A, Richard C.
Laboratoire
de Photochimie Moleculaire et Macromoleculaire, UMR CNRS No. 6505,
F-63177 Aubiere, France.
Acifluorfen was irradiated
in pure water at various excitation wavelengths and pH values.
Numerous photoproducts were obtained which were identified by
[1H]NMR and/or HPLC-MS/MS. The main reaction pathways were photo-decarboxylation,
photo-cleavage of the ether bonding with formation of phenolic
compounds, photo-dechlorination and photo-Claisen type rearrangement.
Decarboxylation was observed in acidic and neutral media whereas
cleavage of the ether bonding dominated in basic media. The photo-Claisen
type rearrangement only occurred on excitation at short wavelengths.
The quantum yield of photolysis was significantly lower at 313
nm (6.1 x 10(-5)) than at 254 nm (2.0 x 10(-3)). The photoreactivity
of acifluorfen was then studied in conditions approaching environmental
conditions. Acifluorfen was dissolved in pure water, in water
containing humic substances or in a natural water, and exposed
to solar light in June at Clermont-Ferrand (latitude 46 degrees
N). In pure water, the half-life was estimated at 10 days and
photo-decarboxylation accounted for 30% of the conversion. The
presence of humic substances (10 mg litre-1) did not affect the
rate of photo-transformation. However, the half-life of acifluorfen
dissolved in the natural water was only 6.8 days.
PMID: 11455817
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11355639&dopt=Abstract
Indian J Biochem
Biophys. 2000 Dec;37(6):498-505.
Oxidative
stress in cucumber (Cucumis sativus L) seedlings treated with
acifluorfen.
Gupta
I, Tripathy BC.
School of
Life Sciences, Jawaharlal Nehru University, New Delhi 110067,
India.
Treatment of diphenyl
ether herbicide acifluorfen-Na (AF-Na) to intact cucumber (Cucumis
sativus L cv Poinsette) seedlings induced overaccumulation of
protoporphyrin IX in light (75 mumole m-2 s-1). The extra-plastidic
protoporphyrin IX accumulated during the light exposure disappeared
within two hours of transfer of acifluorofen-treated seedlings
to darkness. The dark disappearance was due to re-entry of migrated
protoporphyrin IX into the plastid and its subsequent conversion
to protochlorophyllide. In light, protoporphyrin IX acted as a
photosensitizer and caused generation of active oxygen species.
The latter caused damage to the cellular membranes by peroxidation
of membrane lipids that resulted in production of malondialdehyde.
Damage to the plastidic membranes resulted in damage to photosystem
I and photosystem II reactions. Dark-incubation
of herbicide-sprayed plants before their exposure to light enhanced
photodynamic damage due to diffusion of the herbicide to the site
of action. Compared to control, in treated samples the
cation-induced increases in variable fluorescence/maximum fluorescence
ratio and increase in photosystem II activity was lower due to
reduced grana stacking in herbicide-treated and light-exposed
plants.
PMID: 11355639
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11020479&dopt=Abstract
Eur J Pharmacol.
2000 Oct 13;406(2):171-80.
A key role
for the mitochondrial benzodiazepine receptor in cellular photosensitisation
with delta-aminolaevulinic acid.
Mesenholler
M, Matthews EK.
Department
of Pharmacology, University of Cambridge, Tennis Court Road, CB2
1QJ, Cambridge, UK.
The aim of this study
was to determine the part played by the mitochondrial benzodiazepine
receptor in cellular photosensitisation with the protoporphyrin
IX precursor, delta-aminolaevulinic acid. Evaluation of the delta-aminolaevulinic
acid-concentration dependence and kinetics of fluorescent protoporphyrin
IX accumulation in monolayers of rat AR4 2J pancreatoma cells
established a basis for assessing pharmacological modulation of
the biosynthetic pathways for protoporphyrin IX production and
photocytotoxicity. Iron chelation enhanced the accumulation of
photo-active protoporphyrin IX whereas 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxam
ide (PK11195), dipyridamole, or 7-(dimethylcarbamoloxy)-6-phenylpyrrolo-[2,1-d]benzothiazepi
ne (DPB), competitive ligands of the mitochondrial benzodiazepine
receptor, all diminished protoporphyrin
IX accumulation, as did acifluorfen, a mitochondrial protoporphyrinogen
oxidase inhibitor. In addition to protoporphyrin IX (Em(max):
630 nm), delta-aminolaevulinic acid-treated cells also generated
a fluorophore of Em(max) 580 nm; this compound was identified
as Zn-protoporphyrin IX. Mitochondrial benzodiazepine receptor
ligands increased the formation of the zinc porphyrin whilst decreasing
that of protoporphyrin IX. The involvement of the mitochondrial
benzodiazepine receptor in the translocation of porphyrins and
the formation of Zn-protoporphyrin IX have wide implications for
the use of delta-aminolaevulinic acid in photodynamic therapy.
PMID: 11020479
[PubMed - indexed for MEDLINE]
Trends in Plant Science Volume 5, Issue 7 , 1 July 2000,
Page 277
Resistance to the herbicide acifluorfen
G. E. de Vries
Available online 7 July 2000.
The first wave of herbicide resistant crops included those with
resistance to glyphosate, glufosinate and bromoxynil, representing
three different modes of action: disrupting aromatic amino acid
biosynthesis, ammonium assimilation and photosynthesis. Acifluorfen
inhibits protoporphyrinogen IX oxidase (PPOX), an enzyme that
catalyzes a step in the common tetrapyrrole pathway leading to
the synthesis of chlorophyll, and has a rapid action because of
the destruction of cell membranes by oxygen radicals.
Recent work has demonstrated that resistance to the herbicide
acifluorfen can be achieved by overexpression of the target enzyme.
Plant Physiol. (2000) 122, 75–83.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9578577&dopt=Abstract
Biochemistry.
1998 May 12;37(19):6905-10.
Human protoporphyrinogen
oxidase: relation between the herbicide binding site and the flavin
cofactor.
Birchfield
NB, Latli B, Casida JE.
Department
of Environmental Science, University of California, Berkeley 94720-3112,
USA.
Protoporphyrinogen
IX oxidase (protox) catalyzes the oxidation of protoporphyrinogen
IX to protoporphyrin IX in the penultimate step of heme and chlorophyll
biosynthesis in animals and plants. Protox is the target of light-dependent
peroxidizing herbicides and is inhibited at nanomolar levels by
several chemical classes including tetrahydrophthalimides (discussed
below) and diphenyl ethers (e.g., acifluorfen)
usually with little selectivity between the mammalian and plant
enzymes. The herbicide binding site is examined here with a photoaffinity
radioligand optimized on the basis of structure-activity relationships.
A radiosynthetic procedure is described for this new herbicidal
probe, N-(5-azido-4-chloro-2-fluorophenyl)-3,4,5, 6-[3H]tetrahydrophthalimide
([3H]AzTHP), resulting in high specific activity (2.6 TBq/mmol).
Human protox expressed in Escherichia coli and purified by affinity
chromatography is used with [3H]AzTHP to characterize the herbicide/substrate
binding site. Specific binding of [3H]AzTHP to human protox is
rapid, completely reversible in the absence of light with a Kd
of 93 nM, and competitively inhibited by the 5-propargyloxy analogue
and by acifluorfen, which are known
to bind at the substrate (protoporphyrinogen) site. The Bmax establishes
one [3H]AzTHP binding site per FAD. Diphenyleneiodonium, proposed
to inhibit protox by interaction with the FAD cofactor, inhibits
enzyme activity by 48% at 100 micro M without affecting [3H]AzTHP
binding in the presence or absence of substrate, suggesting that
the herbicide binding site may not be proximal to FAD. The first
step has been taken in photoaffinity labeling the herbicide/substrate
site with [3H]AzTHP resulting in apparent covalent derivatization
of 13% of the herbicide binding site.
PMID: 9578577
[PubMed - indexed for MEDLINE]
Toxicology Letters Volume 95, Supplement 1 , July 1998,
Pages 142-143
Effects of diphenyl-ether herbicides on human
erythropoiesis in vitro
B. Rio (a), J. Guinard-Flament (a), A.
Boucher (a) and D. Parent-Massin (a)
a Laboratoire de Microbiologie et Sécurité Alimentaire,
ESMISAB/ISAMOR, Technopôle Brest-Iroise 29280 Plouzanë
France
Oxyfluorfen and acifluorfen, two diphenyl-ether herbicides,
exert their phytotoxic activity preventing chlorophyll synthesis
in plants. They inhibit protoporphyrinogen oxidase, the last enzyme
of the common pathway for chlorophyll and heme synthesis. The
aim of this work was to determine if these herbicides could inhibit
human protoporphyrinogen oxidase during porphyrin and heme synthesis
taking part in hemoglobin formation. Thus, they could induced
metabolic diseases such as Porphyria, characterized by porphyrin
accumulation.
The in vitro evaluation of hematotoxicity due to diphenyl-ether
herbicides was performed on human cells, using an erythroblastic
progenitor culture model. BFU-E/CFU-E are erythroblastic progenitors
able to proliferate and differentiate in vitro to form colonies
of hemoglobinized erythroblasts, under growth factor influence.
Progenitors from human umbilical cord blood obtained from placentas
after normal deliveries, were cultured in semi-solid medium, in
the presence of increasing concentrations of acifluorfen or oxyfluorfen.
BFU-E/CFU-E development was appreciated by morphological analysis
of cell colonies obtained after 14 days of incubation in the presence
of acifluorfen or oxyfluorfen. Spectrophotometric and chromatographic
techniques were used to evaluate cells abilities to synthetize
proteins, porphyrins and hemoglobin, in the presence of diphenyl-ethers.
Results showed that two molecules in the same class of herbicides,
acting by the same mode of action, but differing only by the presence
of a carboxyl group in acifluorfen and an ethoxy group in oxyfluorfen,
did not develop the same effect in human. Even
though the two molecules were cytotoxic for human BFU-E/CFU-E
proliferation, for the same concentration (10-3 M), they did not
exhibit the same effect on differentiation. In contrast
to acifluorfen, oxyfluorfen was able to inhibit hemoglobin synthesis,
in vitro. Thin layer chromatography revealed an absence of heme
and the presence of porphyrins in cells exposed to 10-4 M of oxyfluorfen.
Porphyrins were separated and identified: 10-4 M of oxyfluorfen
induced porphyrin accumulation in erythroblastic progenitors.
Oxyfluorfen could act on hemoglobin synthesis as diphenyl-ethers
act chlorophyll synthesis in plant, by inhibition of protoporphyrinogen
oxidase.
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9007836&dopt=Abstract
Naunyn Schmiedebergs
Arch Pharmacol. 1997 Jan;355(1):8-13.
Regulation
of CYP 2 A 5 induction by porphyrinogenic agents in mouse primary
hepatocytes.
Salonpaa
P, Kottari S, Pelkonen O, Raunio H.
Department of Pharmacology
and Toxicology, University of Oulu, Finland.
All cytochrome P450
(CYP) enzymes contain heme as a prosthetic group. In contrast
to other CYP enzymes, murine CYP 2 A 5 is upregulated in vivo
by several agents that disturb cellular heme balance. To test
the hypothesis that porphyrinogenic agents have the common feature
of being able to increase CYP 2 A 5 expression, mouse liver primary
hepatocytes were exposed to various porphyrinogenic chemicals
and changes in CYP 2 A 5 catalytic activity and levels of mRNA
were monitored. Phenobarbital increased hepatic CYP 2 A 5-mediated
coumarin 7-hydroxylase (COH) activity (13.2-fold) and the amount
of CYP 2 A 5 steady-state mRNA (10.6-fold). Hepatocyte COH activity
was increased also by the ferrochelatase inhibitor griseofulvin
and the protoporphyrinogen oxidase inhibitor acifluorfen
(about 9-fold induction). Of these inducers, only phenobarbital
affected CYP 1 A 12 and CYP 2 B 10 expression. In contrast, many
other porphyrinogenic agents such as cobalt, 2,2,4-trimethyl-1,2-dihydroquinoline
(TMDQ), 1-[4-(3-acetyl-2,4,6-trimethylphenyl)-2,6-cyclohexanedionyl]-O-eth
yl propionaldehyde oxime (ATMP), aminotriazole, and thioacetamide
either decreased or had no effect on CYP 2 A 5. The increases
in COH activity and CYP 2 A 5 mRNA were unaffected by combined
treatment with the inducers and heme arginate, suggesting that
heme is not a regulator of CYP 2 A 5 induction. Treatment with
actinomycin D totally abolished both constitutive CYP 2 A 5 expression
and its inducibility, suggesting that a transcriptional component
is involved. These data suggest that, in mouse primary hepatocytes,
CYP 2 A 5 induction is not a universal response to disturbed cellular
heme biosynthesis.
PMID: 9007836
[PubMed - indexed for MEDLINE]
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]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8761738&dopt=Abstract
Res Microbiol.
1996 Mar-Apr;147(3):193-9.
Identification
of spore-forming strains involved in biodegradation of acifluorfen.
Fortina
MG, Acquati A, Ambrosoli R.
Dipartimento
di Scienze e Tecnologie Alimentari e Microbiologiche, Universita
degli Studi di Milano, Italy.
We isolated and identified
four spore-forming bacteria from activated sludges and soil, three
of which were able to degrade acifluorfen. Biochemical characteristics,
DNA base composition and DNA-DNA homology indicated that the degrading
strains belonged to the species Bacillus thuringiensis, Clostridium
perfringens and Clostridium sphenoides. The fourth strain, identified
as C. sphenoides and showing the same characteristics of the corresponding
degrading strain, was unable to metabolize acifluorfen. Thus,
the plasmid content of these strains was analysed to study the
possible correlation between the presence of extrachromosomal
elements and the ability to degrade this herbicide.
PMID: 8761738
[PubMed - indexed for MEDLINE]
Full
free text available at http://www.jbc.org/cgi/reprint/269/51/32085.pdf
J Biol Chem.
1994 Dec 23;269(51):32085-91.
Purification
and properties of protoporphyrinogen oxidase from the yeast Saccharomyces
cerevisiae. Mitochondrial location and evidence for a precursor
form of the protein.
Camadro JM, Thome F, Brouillet N, Labbe
P.
Departement
de Microbiologie, Institut Jacques Monod, Paris, France.
Protoporphyrinogen
oxidase, the molecular target of diphenylether-type herbicides,
was purified to homogeneity from yeast mitochondrial membranes
and found to be a 55-kDa polypeptide with a pI of 8.5 and a specific
activity of 40,000 nmol of protoporphyrin/h/mg of protein at 30
degrees C. The Michaelis constant (Km) for protoporphyrinogen
IX was 0.1 microM. Due to the high affinity of the enzyme toward
oxygen, the Km for oxygen could only be approximated to 0.5-1.5
microM. The purified enzyme contained a flavin as cofactor. Studies
with rabbit antibodies to yeast protoporphyrinogen oxidase showed
that the enzyme is synthesized as a high molecular weight precursor
(58 kDa) that is rapidly converted in vivo to the mature (55 kDa)
membrane-bound form. Protoporphyrinogen oxidase activity was found
only in purified yeast mitochondrial inner membrane (not in the
outer membrane). Acifluorfen-methyl, a potent diphenylether-type
herbicide, competitively inhibited the purified enzyme (Ki = 10
nM). The mixed inhibition by acifluorfen-methyl
previously reported for the membrane-bound protoporphyrinogen
oxidase (Camadro, J.M., Matringe, M., Scalla, R., and Labbe, P.
(1991) Biochem. J. 277, 17-21) was shown to be related to partial
proteolysis of the enzyme.
PMID: 7798202
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7697001&dopt=Abstract
Biochem Mol
Biol Int. 1994 Dec;34(6):1283-9.
Inhibition
of mammalian protoporphyrinogen oxidase by acifluorfen.
Corrigall
AV, Hift RJ, Adams PA, Kirsch RE.
UCT/MRC Liver
Research Centre, Department of Medicine, South Africa.
We have studied the
kinetics of the inhibition of mitochondrial protoporphyrinogen
oxidase (PPO) from liver and placenta of 3 mammalian species by
the diphenyl ether herbicide acifluorfen (AF). AF competitively
inhibited PPO from human liver and placenta, mouse liver and pig
placenta with respect to its substrate protoporphyrinogen. In
contrast, mixed-type inhibition was shown for pig liver. The differing
results shown in pig liver may point to structural differences
in PPO derived from different species and tissues. We have also
compared the effects of AF on the function of PPO in human lymphoblasts
from normal subjects and those with variegate porphyria, an inherited
disorder of PPO. Competitive inhibition was shown for both and
there were no significant differences in the values of Ks or Ki.
PMID: 7697001
[PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8451878&dopt=Abstract
Zentralbl
Mikrobiol. 1993 Jan;148(1):16-23.
Microbial
biomass-persistence relationships of acifluorfen in a clay-loam
soil.
Perucci
P, Scarponi L.
Istituto Chimica
Agraria, Universita di Perugia, Italy.
The interference of
the effect of the herbicide acifluorfen on microbial biomass and
on hydrolytic capacity, and its persistence in a clay-loam soil
before and after enrichment with glucose, were investigated. The
experiment was carried out under laboratory conditions for 120
days. Acifluorfen was added to the soil at two different application
rates corresponding to 1X and 10X the recommended field rate.
Biomass-C was significantly higher in the enriched soil during
the first 35 days; subsequently there was a tendency to return
to the original value of the unenriched soil. The herbicidal treatments
depressed the biomass-C level, particularly at the higher rate.
The hydrolytic capacity, measured as FDA-hydrolase activity, was
significantly higher in the enriched soil than in the unenriched
soil. This was enhanced by acifluorfen treatment, chiefly at the
higher rate. The degradation trend of acifluorfen was not significantly
different at the two rates, but was significantly faster in the
enriched soil. Half-life values of 28 and 40 days were found in
the enriched and unenriched soil, respectively.
PMID: 8451878
[PubMed - indexed for MEDLINE]
PESTIC BIOCHEM PHYSIOL; 42 (3). 1992.
271-278.
Effects of light and ethylene on the herbicidal
action of acifluorfen.
Acifluorfen CAS No. 50594-66-6
ABDALLAH M MF, BAYER DE, ELMORE CL
Ain Shams Univ., Cairo, Egypt.
BIOSIS COPYRIGHT: BIOL ABS. Fully expanded cotyledons from 7-day-old
cucumber (Cucumis sativis L. cv Ashy) seedlings were used to study
the interaction of light and ethylene on the herbicidal action
of acifluorfen (5-(2-chloro-4-(trifluoromethyl)phenoxy)-2-nitrobenzoic
acid). Acifluorfen alone increased the level of ethylene production
from cucumber cotyledons. The stimulation was most pronounced
after 12 hr in the light as compared to continuous dark. The evolution
of ethylene induced by acifluorfen was complete by 48 hr after
treatment. Symptoms resulting from acifluorfen treatment developed
rapidly in light, while no visible symptoms developed in the dark
treatment. Cotyledons treated with acifluorfen showed a corresponding
increase in carbon dioxide production. An ethylene inhibitor,
alpha-aminooxyacetic acid (AOA), inhibited ethylene production
in acifluorfen-treated cucumber cotyledons. In addition it reduced
the visual injury induced by this herbicide. Cucumber cotyledons
treated with AOA a [abstract truncated]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1404247&dopt=Abstract
J Biochem
Toxicol. 1992 Summer;7(2):87-95.
Effects
of diphenyl ether herbicides on porphyrin accumulation by cultured
hepatocytes.
Jacobs
JM, Sinclair PR, Gorman N, Jacobs NJ, Sinclair JF, Bement WJ,
Walton H.
Department
of Microbiology, Dartmouth Medical School, Hanover, New Hampshire
03756.
Several diphenyl ether
herbicides, such as acifluorfen methyl, have been previously shown
to cause large accumulations of the heme and chlorophyll precursor,
protoporphyrin, in plants. Light-induced herbicidal damage is
mediated by the photoactive porphyrin. Here we investigate whether
diphenyl ether herbicides can affect porphyrin synthesis in rat
and chick hepatocytes. In rat hepatocyte cultures, protoporphyrin,
as well as coproporphyrin, accumulated after treatment with acifluorfen
or acifluorfen methyl. Combination of acifluorfen methyl with
an esterase inhibitor to prevent the conversion of acifluorfen
methyl to acifluorfen resulted in a greater accumulation of porphyrins
than caused by acifluorfen methyl or acifluorfen alone. In vitro
enzyme studies of hepatic mitochondria isolated from rat and chick
embryos demonstrated that protoporphyrinogen oxidase, the penultimate
enzyme of heme biosynthesis, was inhibited by low concentrations
of acifluorfen, nitrofen, or acifluorfen methyl with the latter
being the most potent inhibitor. These findings indicate that
diphenyl ether treatment can cause protoporphyrin accumulation
in rat hepatocyte cultures and suggest that this accumulation
was associated with the inhibition of protoporphyrinogen oxidase.
In cultured chick embryo hepatocytes, treatment with acifluorfen
methyl plus an esterase inhibitor caused massive accumulation
of uroporphyrin rather than protoporphyrin or coproporphyrin.
Specific isozymes of cytochrome P450 were also induced in chick
embryo hepatocytes. These effects were not observed in the absence
of an esterase inhibitor. These results suggest that diphenyl
ether herbicides can cause uroporphyrin accumulation similar to
that induced by other cytochrome P450-inducing chemicals such
as polyhalogenated aromatic hydrocarbons in the chick hepatocyte
system.
PMID: 1404247
[PubMed - indexed for MEDLINE]
ENVIRON MUTAGEN 5:435,1983
DEVELOPMENT OF AN IN VITRO ASSAY FOR
TERATOGENICITY USING HUMAN LYMPHOCYTES
FRANCIS BM, PLEWA MJ, ENGL SA
Taxonomic Name: HOMO SAPIENS
Test Object: MAMMAL, HUMAN CELL CULTURE
Tissue Cultured: LYMPHOCYTES
Experimental Conditions: IN VITRO
Name of Agent (CAS RN):
NITROFEN ( 1836-75-5 )
BIFENOX ( 42576-02-3 )
OXYFLUORFEN ( 42874-03-3 )
ACIFLUORFEN ( 50594-66-6 )
MICROSOMES,RAT LIVER,S9
SODIUM FLUORIDE ( 7681-49-4 )
METABOLIZING SYSTEM
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