Degradation of Benthiocarb Herbicide in Soil

Ishikawa, Kanji; Nakamura, Yasuo; Kuwatsuka, Shozo

doi:10.1584/jpestics.1.49

Cited by 20 publications

(5 citation statements)

References 3 publications

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“…The major metabolic pathway for thiocarbamate herbicides in rats involves sulfoxidation, and then GSTcatalyzed conjugation with GSH, leading to excretion of the mercapturate (20) and release of the appropriate sulfenic acid, which is decomposed or reduced to the thiol (34). S-Methyl thioether metabolites (or their sulfoxides and sulfones), as identified in this study with mice, have been previously demonstrated for thiobencarb in soil (35) and triallate in rats (36). Identification of the S-methyl analog of molinate as a metabolite of the GSH conjugate of molinate indicates that conjugation of thiocarbamates with GSH does not always lead to their irreversible detoxification.…”

Section: Discussionsupporting

confidence: 61%

S-methylation as a bioactivation mechanism for mono- and dithiocarbamate pesticides as aldehyde dehydrogenase inhibitors

Staub¹,

Sparks²,

Quistad³

et al. 1995

Chem. Res. Toxicol.

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S-Methylation is a new bioactivation mechanism for metam and metabolites of methyl isothiocyanate and dazomet in mice. These soil fumigants are converted to S-methyl metam [MeNHC(S)SMe] which reaches peak levels in liver, kidney, brain, and blood 10-20 min after intraperitoneal (ip) treatment. The half-life of S-methyl metam administered ip is 8-12 min in each of these tissues. S-Methyl metam-oxon [MeNHC(O)SMe] is also detected as a metabolite of each of these soil fumigants on analysis by gas chromatography/mass spectrometry with chemical ionization. The conversion of methyl isothiocyanate to S-methyl metam and its oxon probably involves conjugation with glutathione, hydrolysis to S-(N-methylthiocarbamoyl)-cysteine, cleavage by cysteine conjugate beta-lyase to release metam, and finally methylation and oxidative desulfuration. Metam and dazomet are converted to S-methyl metam by mouse liver microsomes on fortification with S-adenosylmethionine. Metam, methyl isothiocyanate, dazomet, and three metabolites (metam-oxon [MeNHC(O)SH], MeNHC(S)SMe, and MeNHC-(O)SMe) administered ip to mice at 40 mg/kg inhibit low-Km liver mitochondrial aldehyde dehydrogenase and elevate ethanol-dependent blood and brain acetaldehyde levels. Several fungicides including the dialkyldithiocarbamates as the disulfide (thiram and the related alcohol-abuse drug disulfiram) and metal salts (ziram) also yield S-methyl thiocarbamate metabolites. Eight S-alkyl and S-(chloroallyl) thiocarbamate herbicides (EPTC, molinate, butylate, vernolate, pebulate, diallate, sulfallate, and triallate), but not their S-chlorobenzyl analog (thiobencarb), undergo sequential liberation of the thiocarbamic acid and then S-methylation, forming the S-methyl thiocarbamates which are new metabolites and potential aldehyde dehydrogenase inhibitors. The S-methyl mono- and dithiocarbamate metabolites of these herbicides and fungicides are easily identified by retention time on gas chromatography and by mass spectrometry giving [MH]+ plus [R1R2NCO]+ or [R1R2NCS]+, respectively, as the two major ions.

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Section: Discussionsupporting

confidence: 61%

S-methylation as a bioactivation mechanism for mono- and dithiocarbamate pesticides as aldehyde dehydrogenase inhibitors

Staub¹,

Sparks²,

Quistad³

et al. 1995

Chem. Res. Toxicol.

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“…In other rice growing countries, thiobencarb has also been found to be degraded slowly under flooded, anaerobic soil conditions. A half-life of 100 days was determined in flooded Japanese soils, and a half-life of around 200 days was calculated in reduced, flooded conditions in the United States (6,11,35,36).…”

Section: Resultsmentioning

confidence: 99%

“…Information in the literature is available for the persistence of thiobencarb and molinate from laboratory studies ( − ) and in controlled water management conditions ( − ). Some studies on the dissipation of thiobencarb and molinate in commercial rice fields and in agricultural drains have also been conducted ( − ).…”

Section: Introductionmentioning

confidence: 99%

Field Dissipation and Environmental Hazard Assessment of Clomazone, Molinate, and Thiobencarb in Australian Rice Culture

Quayle

Oliver

Zrna

2006

J. Agric. Food Chem.

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The fates of clomazone [2-(2-chlorophenyl)methyl-4,4-dimethyl-3-isoxazolidinone], molinate (S-ethyl hexahydro-1-H-azepine-1-carbothioate), and thiobencarb {S-[(4-chlorophenyl)methyl]diethylcarbamothioate} applied to rice were studied at two locations in New South Wales (Australia). Rates of dissipation (DT50) from floodwaters and soils were measured. Dissipation of the three herbicides from water and soil can be best explained by a first-order decay process. DT(50) values for clomazone, molinate, and thiobencarb were 7.2, 5.1, and 3.5 days, respectively, in water and 14.6, 23.9, and >46 days, respectively, in surface soil. Maximum measured concentrations of clomazone, molinate, and thiobencarb in floodwaters were 202, 1042, and 148 microg/L, respectively, taking 18.4, 26.4, and 21.4 days to dissipate to concentrations set to protect aquatic ecosystems. A hazard assessment identified clomazone as presenting a low environmental hazard while molinate and thiobencarb presented a medium environmental hazard when used at registered field rates.

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“…Thiocarbamate herbicides are rapidly degraded in mammals and plants and some metabolites from the S-alkyl or S-benzyl fragments are identified (Ashton and Crafts, 1973;Casida et al, 1974Casida et al, , 1975aFang, 1975;Ishikawa et al, 1973Ishikawa et al, , 1976; Ong and Fang, 1970). Thiocarbamates also undergo N-dealkylation and sulfoxidation in mammals or liver microsomal mixed-function oxidase (mfo) systems (Casida et al, 1974(Casida et al, ,1975aIshikawa et al, 1973).…”

mentioning

confidence: 99%

Metabolic fate of the N,N-dialkylcarbamoyl moiety of thiocarbamate herbicides in rats and corn

Hubbell¹,

Casida²

1977

J. Agric. Food Chem.

102

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A major metabolic pathway for EPTC and butylate in rats, accounting for at least 27-45% of the administered dose, is as follows: thiocarbamate -thiocarbamate sulfoxide -S-(N,N-dialkylcarbamoy1)glutathione -S-(Na-dialkylcarbamoy1)cysteine -S-(Na-dialkylcarbamoy1)mercapturic acid, S-(N,N-dialkylcarbamoy1)mercaptoacetic acid, and N-[S-(N,N-dialkylcarbamoy1)mercaptoacetyllglycine (from butylate only). S-(N-1sobutylcarbamoyl)mercapturic acid is also formed from butylate. These findings are based on identification and quantitation of the urinary metabolites from 14CO-labeled preparations of the first four compounds in the metabolic sequence, in both the EPTC and butylate series. About 40% of the administered [WOIEPTC and ['4@O]butylate dose is metabolized by ester cleavage and 14C02 liberation without going through the thiocarbamate sulfoxide as an intermediate. Benthiocarb, cycloate, molinate, and pebulate also give the appropriate mercapturic acid derivatives in the urine. The roots and leaves of corn seedlings convert [14CO]EPTC or ita sulfoxide to the glutathione and cysteine conjugates and many other metabolites that are the same compounds in control plants and those treated with the antidote, R-25788.

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Degradation of Benthiocarb Herbicide in Soil

Cited by 20 publications

References 3 publications

S-methylation as a bioactivation mechanism for mono- and dithiocarbamate pesticides as aldehyde dehydrogenase inhibitors

S-methylation as a bioactivation mechanism for mono- and dithiocarbamate pesticides as aldehyde dehydrogenase inhibitors

Field Dissipation and Environmental Hazard Assessment of Clomazone, Molinate, and Thiobencarb in Australian Rice Culture

Metabolic fate of the N,N-dialkylcarbamoyl moiety of thiocarbamate herbicides in rats and corn

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