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NTIS/PB97-144125
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Available
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1997
- Pesticide Fact Sheet: Thiazopyr.
Environmental Protection Agency, Washington, DC. Office
of Prevention, Pesticides and Toxic Substances. |
This
document contains up-to-date chemical information, including
a summary of the Agency's regulatory position and rationale,
on a specific pesticide or group of pesticides. A Fact
Sheet is issued after Registration of a new chemcial. |
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11407034&dopt=Abstract
Pest Manag
Sci 2001 Jun;57(6):560-3
Adsorption
and degradation of thiazopyr in compost-amended and non-amended
soils.
Fernandez MD, Sanchez-Brunete
C, Rodriguez AJ, Tadeo JL.
Department of Sustainable Use of Natural Resources,
INIA, Apartado 8111, 28080 Madrid, Spain.
Adsorption and degradation of thiazopyr on two
unamended soils and a soil amended annually during 8 years with
compost were studied under laboratory conditions and compared
with the results obtained on soils amended with fresh sewage
sludge compost. The adsorption isotherms fitted the Freundlich
equation well and a marked sorption increase was found in amended
soils. Degradation data followed first-order kinetics and thiazopyr
had a half-life of about 75 days at 25 degrees C and 60% water-holding
capacity of soil. The addition of fresh
compost markedly decreased the rate of thiazopyr degradation,
whereas the compost mineralised in the field after annual additions
had only a small influence. Incubation studies with sterile
soils showed a very significant decrease of the degradation
rate, indicating that degradation by micro-organisms was the
main pathway of thiazopyr degradation in the soils studied.
PMID: 11407034 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9681970&dopt=Abstract
Environ
Health Perspect 1998 Aug;106(8):437-45
Mode
of carcinogenic action of pesticides inducing thyroid
follicular cell tumors in rodents.
Hurley PM.
Office of Prevention, Pesticides and Toxic Substances,
U.S. Environmental Protection Agency,
Washington, DC 20460 USA.
Of 240 pesticides screened for carcinogenicity by the U.S. Environmental
Protection Agency Office of Pesticide Programs, at least 24
(10%) produce thyroid follicular cell tumors in rodents. Thirteen
of the thyroid carcinogens also induce liver tumors, mainly
in mice, and 9 chemicals produce tumors at other sites. Some
mutagenic data are available on all 24 pesticides producing
thyroid tumors. Mutagenicity does not seem to be a major determinant
in thyroid carcinogenicity, except for possibly acetochlor;
evidence is less convincing for ethylene thiourea and etridiazole.
Studies on thyroid-pituitary functioning, including indications
of thyroid cell growth and/or changes in thyroxine, triiodothyronine,
or thyroid-stimulating hormone levels, are available on 19 pesticides.
No such antithyroid information is available for etridiazole,
N-octyl bicycloheptene dicarboximide, terbutryn, triadimefon,
and trifluralin. Of the studied chemicals, only bromacil lacks
antithyroid activity under study conditions. Intrathyroidal
and extrathyroidal sites of action are found: amitrole, ethylene
thiourea, and mancozeb are thyroid peroxidase inhibitors; and
acetochlor, clofentezine, fenbuconazole, fipronil, pendimethalin,
pentachloronitrobenzene, prodiamine, pyrimethanil, and thiazopyr
seem to enhance the hepatic metabolism and excretion of thyroid
hormone. Thus, with 12 pesticides that mode of action
judgments can be made, 11 disrupt thyroid-pituitary homeostasis
only; no chemical is mutagenic only; and acetochlor may have
both antithyroid and some mutagenic activity. More information
is needed to identify other potential antithyroid modes of thyroid
carcinogenic action.
PMID: 9681970 [PubMed - indexed
for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9007042&dopt=Abstract
Toxicol
Appl Pharmacol 1997 Jan;142(1):133-42
Mechanism
of thiazopyr-induced effects on thyroid
hormone homeostasis in male Sprague-Dawley rats.
Hotz KJ, Wilson AG, Thake DC,
Roloff MV, Capen CC, Kronenberg JM, Brewster DW.
Monsanto Company, St. Louis, Missouri
63167, USA.
Chronic administration of thiazopyr in the diet at dose levels
of 1000 and 3000 ppm, but not 100 ppm, has demonstrated an increase
in thyroid follicular cell tumors in male
Sprague-Dawley rats. In the studies reported here we
have evaluated the mechanism of thiazopyr-induced thyroid tumors
by studying the effect of thiazopyr on a number of endpoints
that indicate hypothalamic-pituitary-thyroid homeostasis. At
a dose level of 3000 ppm, thiazopyr caused
a marked depression in circulating levels of T4 as soon as 7
days after commencement of treatment. Concurrent with this decrease
in T4 was an increase in TSH levels, an increase in thyroid
and liver weights, a three- to sixfold increase in hepatic T4-uridine
diphosphate glucuronosyl transferase (UDPGT) activity, and increases
in thyroid follicular cell hypertrophy and hyperplasia.
Dose-related changes associated with thiazopyr treatment were
significant increases in liver weight,
thyroid weight, and hepatic T4-UDPGT activity at high doses.
Increased levels of serum TSH, T3, and rT3, decreased levels
of T4, and an increased incidence of thyroid follicular cell
hypertrophy and hyperplasia were observed 56 days after the
initiation of 3000 ppm thiazopyr. All the changes, except
thyroid weight, were partially or completely reversible upon
removal of thiazopyr from the diet. Increased thyroid T4 elimination,
primarily via increased hepatic conjugation by T4-UDPGT, resulting
in decreased serum T4, appeared to be responsible for the increased
TSH levels. The sustained increase in TSH by thiazopyr appears
responsible for the stimulation of the thyroid follicular cells
resulting in follicular cell hypertrophy, hyperplasia, and ultimately
neoplasia. In summary, evidence is presented for a hormonally
mediated, threshold-dependent process for the development of
thyroid follicular cell tumors from high-dose thiazopyr administration
in male rats. This mechanism is not considered to be relevant
to humans, since the thyroid of humans is much less sensitive
to this pathogenic phenomenon than rodents.
PMID: 9007042 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7604604&dopt=Abstract
Xenobiotica
1995 Jan;25(1):27-35
Metabolic
deactivation of the herbicide thiazopyr by animal liver esterases.
Feng PC, Ruff TG, Kosinski WG.
Agricultural Group, Monsanto Co.,
St Louis, MO 63198, USA.
1. Thiazopyr was hydrolysed in vitro to its corresponding acid
by rabbit and porcine liver esterases.
2. A wide range of thiazopyr esterase activity was observed
in extracts from liver acetone powders from 15 animal species
with bovine, rabbit and pigeon showing the highest activities.
3. Using soybean tissue culture cells and Arabidopsis seedlings,
the acidic metabolite was shown to possess < 1% of the herbicidal
activity of thiazopyr.
4. We propose that biotransformation of thiazopyr to the acid
is a critical pathway of metabolism in animals and plants.
PMID: 7604604 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7839696&dopt=Abstract
Xenobiotica
1994 Aug;24(8):729-34
In
vitro biotransformation of thiazopyr by rat liver microsomes:
oxidative cleavage of a carboxylic methylester by monooxygenases.
Feng PC, Solsten RT.
Agricultural Group, Monsanto Co.,
St Louis, MO 63198.
1. Thiazopyr was metabolized by liver microsomes from male Sprague-Dawley
rats to a previously unidentified metabolite.
2. The new metabolite was identified by coelution with an authentic
standard in hplc and by electrospray lc/ms as the corresponding
carboxylic acid.
3. Formation of the carboxylic acid metabolite was inhibited
in the presence of mono-oxygenase inhibitors including piperonyl
butoxide, 1-aminobenzotriazole, metyrapone and tetcyclacis.
4. Transformation of thiazopyr to its carboxylic acid by rat
liver microsomes is mediated by mono-oxygenases and not hydrolases.
PMID: 7839696 [PubMed - indexed for MEDLINE]
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