Abstracts
Thiazopyr
CAS No. 117718-60-2
For more abstracts search PubMed or Toxnet
 
 

ACTIVITY: Herbicide (Pyridinecarboxylic acid)

CAS Name: methyl 2-(difluoromethyl)-5-(4,5-dihydro-2-thiazolyl)-4-(2-methylpropyl)-6-(trifluoromethyl)-3-pyridinecarboxylate

Structure:


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Order No. Title Abstract / Keywords

NTIS/PB97-144125

11p

Available free online

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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