SEARCH · PubMed Health

Results for “Triallate”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

65 records · Page 4Linked to original sources

PubMed1995

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

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.

Aldehyde Dehydrogenase↗

PubMed2003

Toxicity of a complex mixture of atmospherically transported pesticides to Ceriodaphnia dubia.

The presence of several anthropogenic chemicals has been documented in the atmosphere of the Canadian prairies. The deposition of these chemicals as a mixture is of importance since little is known of the combined effects of these chemicals on aquatic organisms. This study was designed to evaluate the acute and chronic toxicity of a complex mixture of nine atmospherically transported pesticides to Ceriodaphnia dubia. The nine selected pesticides (bromoxynil, dicamba, 2,4-D, MCPA, triallate, trifluralin, pentachlorophenol, lindane, and 4,4'-DDT) were detected in appreciable quantities in dry atmospheric deposits. The concentration of each pesticide in the mixture was based on maximum measured daily dry deposition rates for central Canada, except for pentachlorophenol, which was estimated based on atmospheric concentrations. The 48-h LC50 estimate for C. dubia exposed to the pesticide mixture was 174.60 microg L(-1) (340 times the measured total dry deposition concentration). The estimated NOEC and LOEC for both survival and reproduction, as determined in the 7-d chronic toxicity test, were 51.3 (100 times) and 154 microg/L(-1) (300 times), respectively. A basic risk assessment, using the toxic unit approach, suggested that the toxicity of the pesticide mixture was mainly due to 4,4'-DDT. Overall, this atmospherically transported complex mixture of pesticides appears to pose a negligible toxicological risk to non-target aquatic invertebrates such as zooplankton.

Air Pollutants↗

PubMed1980

Mutagenicity evaluation of chemical pesticides.

Over the last few decades, the use of chemical pesticides has increased dramatically in the U.S. This relatively sudden increase greatly concerns the U.S. Environmental Protection Agency (EPA), since it has the responsibility for ensuring the safety of all pesticides used in the U.S. In response to this concern, EPA has established a review program, the Rebuttable Presumption Against Registration (RPAR), for periodically reassessing the mutagenic and carcinogenic potential of pesticide compounds. This paper presents a review and evaluation of the data reported in the literature on six chemical pesticides suspect for mutagenic potential. The pesticide chemicals discussed are maleic hydrazide; rotenone; monuron; diallate; triallate, and benomyl.

Animals↗

PubMed2003

Factors associated with detection of bromoxynil in a sample of rural residents.

In regions of intensive crop production residents may be exposed to herbicides through direct contact or environmental sources. The environmental herbicide exposures of rural populations and resultant potential health effects are not well understood. Epidemiologic studies or herbicides have focused on occupational exposures using, primarily, self-reported data (e.g., information on occupational and non-occupational herbicide use, agricultural practices and exposures, farm residence). Herbicide exposure characterization in epidemiologic research would be strengthened by the use of self-reported data and biological monitoring (e.g. measuring the herbicide parent compound or its metabolites in blood or urine specimens) to classify individual exposures, identify factors associated with exposure, and obtain integrated estimates of exposure. As both exposure metrics are susceptible to measurement error and some self-reported and biological monitoring data might not be correlated, a worthwhile first step is to identify self-reported data that are statistically associated with biological measures or exposure. This study use gas chromatography/mass spectrometry analysis to measure blood plasma concentrations of target herbicides in a sample of rural residents (men, women, and youths) of Saskatchewan, Canada, and identified factors, based on self-reported data, associated with detection. The questionnaire data and blood specimens were collected in February/March 1996 during winter (frozen soil and water and snow cover) conditions. Sixty-four of the 332 study participants (19.3%) had detectable levels of the herbicide bromoxynil although herbicide application in the region had not occurred for approximately 5 mo and bromoxynil has a relatively short environmental half-life. The prevalence of detection of other target herbicides (2,4-D, triallate, trifluralin, dicamba, fenoxaprop, MCPA, and ethalfluralin) varied from 0.3% to 2.7%. Self reported factors identified in the multiple-variable analysis as statistically significant predictors of bromoxynil detection included recent exposure to grain production as the main farming operation (statistically significant for producers and for non-farming family members of producers), a history of bromoxynil use, a history of having felt ill with a pesticide exposure and a history of pesticide spill on skin or clothing, with apparent gender differences in the relative importance of these factors. Detection of bromoxynil in this rural sample, 3-4 mo after freeze-up and winter snow cover, suggests either that bromoxynil is very slowly metabolized/excreted from the body or study participants were environmentally or occupationally exposed tothe herbicide during this period. Further research is needed to elucidate the pathways of exposure, biological half-life, and potentialhuman health effects of bromoxynil.

Adolescent↗

PubMed1982

Significance of plant metabolism in the mutagenicity and toxicity of pesticides.

In an attempt to gain an overall estimate for the influence of plant metabolism on environmental mutagenesis, the mutagenicity of an assortment of agricultural pesticide preparations in the Salmonella bio-assay was evaluated using both rat liver S9 and plant enzyme homogenates as activating systems. The study indicates that plant metabolism can alter the results of this short-term mutagenicity test: some compounds which are non mutagenic in the Salmonella bio-assay (e.g. diquat) give positive responses, some preparations such as captan become more or less mutagenic, and some, such as triallate, become significantly more toxic to the tester strains. Furthermore, dose response curves suggest that even when both plant homogenates and rat liver S9 supernatant activate a compound, the mutagens which are formed may differ. Five-day old alfalfa (Medicago sativa L.), corn (Zea mays L. var. Golden Jubilee), bean (Vicia faba L), pea (Pisum sativum L. var. Laxton's Progress), sunflower (Helianthus annuus var. Krasnodarets), tobacco (Nicotiana tobaccum L. var. Wisconsin 58), and wheat (Triticum aestivum L.) were tested and compared as activating systems; these were prepared by an assortment of cell disruption techniques including blending, homogenizing, sonication, and high pressure disruption methods. For routine testing, filter sterilized, blended, S14 supernatants of corn or wheat were the most promising. No correlation was observed between levels of activation by the various plant species and their protein contents, catalase, or peroxidase activities. The preparations, however, could be standardized using specific chemical compounds in the bio-assay.

Animals↗

PubMed2000

Inhibition of cellular action of thrombin by N3-cyclopropyl-7-[[4-(1-methylethyl)phenyl]methyl]-7H-pyrrolo[3, 2-f]quinazoline-1,3-diamine (SCH 79797), a nonpeptide thrombin receptor antagonist.

A growing body of evidence suggests an important contribution of the cellular actions of thrombin to thrombosis and restenosis following angioplasty. Recently we reported on SCH 79797 (N3-cyclopropyl-7-¿[4-(1-methylethyl)phenyl]methyl¿-7H-pyrrolo[3, 2-f]quinazoline-1,3-diamine) and its analogs as new potent, nonpeptide thrombin receptor antagonists. This study further characterizes the biochemical and pharmacological actions of pyrroloquinazoline inhibitors of protease activated receptor-1 (PAR-1) in human platelets and coronary artery smooth muscle cells (hCASMC). SCH 79797 and its N-methyl analog (SCH 203099) inhibited binding of a high-affinity thrombin receptor-activating peptide ([(3)H]haTRAP, Ala-Phe(p-F)-Arg-ChA-HArg-[(3)H]Tyr-NH(2)) to PAR-1 with IC(50) values of 70 and 45 nM, respectively. SCH 79797 inhibited [(3)H]haTRAP binding in a competitive manner. SCH 79797 and SCH 203099 inhibited alpha-thrombin- and haTRAP-induced aggregation of human platelets, but did not inhibit human platelet aggregation induced by the tethered ligand agonist for protease-activated receptor-4 (PAR-4), gamma-thrombin, ADP, or collagen. SCH 203099 inhibited surface expression of P-selectin induced by haTRAP and thrombin, and it did not increase P-selectin expression or prevent thrombin cleavage of the receptor. Thrombin and TFLLRNPNDK-NH(2) (TK), a PAR-1-selective agonist, produced transient increases in cytosolic free Ca(2+) concentration ([Ca(2+)](i)) in hCASMC. This increase in [Ca(2+)](i) was inhibited effectively by SCH 79797. However, the Ca(2+) transients induced by SLIGKV-NH(2,) a PAR-2-selective agonist, were not inhibited by SCH 79797. Thrombin- and TK-stimulated [(3)H]thymidine incorporation also was inhibited completely by SCH 79797. The results of this study demonstrate that SCH 79797 and SCH 203099 are potent, selective antagonists of PAR-1 in human platelets and hCASMC. These data also suggest that the thrombin stimulation of Ca(2+) transients and mitogenesis in hCASMC is mediated primarily through activation of PAR-1.

Apoptosis Regulatory Proteins↗

PubMedDate not supplied