2 edition of Pharmacokinetics of trichloroethylene and its metabolites in the rat found in the catalog.
Pharmacokinetics of trichloroethylene and its metabolites in the rat
Peter Lawrence Bonate
Written in English
|Statement||by Peter Lawrence Bonate.|
|The Physical Object|
|Pagination||viii, 45 leaves, bound :|
|Number of Pages||45|
The embryotoxicity of trichloroethylene (TRI) tetrachloroethylene (PER), and of four of their oxidative metabolites i.e. trichloroacetic acid, dichloroacetic acid, chloral hydrate, and trichloroacetyl chloride, was studied in vitro, using the rat whole embryo culture system. Embryos from Sprague-Dawley rats were explanted on gestational day 10 (plug day=day 0) and cultured for 46 h in the Cited by: Trichloroethylene (TCE) is an occupational and ubiquitous environmental contaminant, and TCE exposure will increase the risk of autoimmune diseases and allergic diseases. T cells play an important role in the pathogenesis of TCE-related immune disorders, but the effect of TCE and its oxidative metabolites, trichloroacetic acid (TCA) and dichloroacetic acid (DCA), on the activation of human T Cited by: 3.
A six-compartment physiologically based pharmacokinetic (PBPK) model for the B6C3F1 mouse was developed for trichloroethylene (TCE) and was linked with five metabolite submodels consisting of four compartments each. The PBPK model for TCE and the metabolite submodels described oral uptake and metabolism of TCE to chloral hydrate (CH). A physiologically based pharmacokinetic (PBPK) model for inhaled trichloroethylene (TCE) was developed for B6C3F 1 mice. Submodels described four Pmediated metabolites of TCE, which included chloral hydrate (CH), free and glucuronide-bound trichloroethanol (TCOH-fand TCOH-b), trichloroacetic acid (TCA), and dichloroacetic acid (DCA).Inhalation time course studies were carried Cited by:
Trichloroethylene and its breakdown products (metabolites) can be measured in blood and urine. However, the detection of trichloroethylene or its metabolites cannot predict the kind of health effects that might develop from that exposure, partly because exposure to other chemicals can produce byproducts similar to those observed following. Abstract. Trichloroethylene (TCE) is a well-known carcinogen in rodents and concerns exist regarding its potential carcinogenicity in humans. Oxidative metabolites of TCE, such as dichloroacetic acid (DCA) and trichloroacetic acid (TCA), are thought to be hepatotoxic and carcinogenic in mice.
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Much progress has been made in understanding the complex pharmacokinetics of trichloroethylene (TCE). Qualitatively, it is clear that TCE is metabolized to multiple metabolites either locally or into systemic circulation.
Many of these metabolites are thought to have toxicologic by: A physiologically based pharmacokinetic (PB-PK) model was developed to describe trichloroethylene (TCE) kinetics in the lactating rat and nursing pup.
The lactating dam was exposed to TCE either by inhalation or by ingestion in drinking water. The nursing pup's exposure to TCE was by ingestion of maternal milk containing by: Blood level kinetics of trichloroethylene and its metabolites confirmed a faster rate of metabolism in the mouse than in the rat.
Peak concentrations of the metabolites were reached within 2 hr of dosing in the mouse compared to 10 to 12 hr in the rat. The concentrations of both trichloroethanol (4X) and trichloroacetic acid (7X) were significantly higher in the mouse than in the by: Chiu W, Okino M, Lipscomb J and Evans M () Issues in the Pharmacokinetics of Trichloroethylene and Its Metabolites, Environmental Health Perspectives,(), Online publication date: 1-SepCited by: A physiologically based pharmacokinetic model for trichloroethylene and its metabolites, chloral hydrate, trichloroacetate, dichloroacetate, trichloroethanol, and trichloroethanol glucuronide in B6C3F1 mice.
by: This article has been cited byother articles in PMC. Abstract. A major focus in the study of metabolism and disposition of trichloroethylene (TCE) is to identify metabolites that can be used reliably to assess flux through the various pathways of TCE metabolism and to identify those metabolites that are causally associated with toxic responses.
Another important issue involves delineation of sex- and species Cited by: The pharmacokinetics of trilostane and one of its metabolites ketotrilostane are described and characterized in the rat following the separate intravenous administration of trilostane and ketotrilostane.
It was noted during these studies that the parent compound and its metabolite undergo metabolic interconversion–trilostane producing ketotrilostane and ketotrilostane generating by: 7.
Although TCE was detected in rat fetuses following maternal exposure to TCE, metabolites were utilized in the present study because most TCE is rapidly metabolized Cited by: 8. Recent PBPK models for TCE and its metabolites have focused on the major metabolic pathway for metabolism of TCE (Pmediated metabolic pathway).
This article briefly reviews selected published compartmental and PBPK models for TCE. Trichloroacetic acid (TCA) is considered a principle metabolite responsible for TCE-induced liver cancer in by: Abstract. Inhalation pharmacokinetics of the halogenated ethylenes vinyl fluoride (VF), vinylidene fluoride (VF 2), vinyl chloride (VC1), vinylidene chloride (VC1 2), cis- and trans-dichloroethylene (cis-DCE and trans-DCE), trichloroethylene (Tri), perchloroethylene (Per), and vinyl bromide (VBr) have been comparatively studied in the were exposed in a closed inhalation system to Cited by: The pharmacokinetics of trichloroethylene (TCE) in male Sprague-Dawley (S-D) rats were characterized (1) during and after inhalation exposure to 50 or ppm TCE, (2) following administration of 8 mg/kg TCE PO, and (3) following intra-arterial injection of 8 mg/kg TCE.
A physiologically based pharmacokinetics (PBPK) model was developed which provides a comprehensive description of the kinetics of trichloroethylene (TCE) and its metabolites, trichloroethanol (TCOH). and trichloroacetic acid (TCA), in the mouse, rat, and human, for both oral and inhalation by: J.W Fisher, T.A Whittaker, D.H Taylor, H.J Clewell III, M.E AndersenPhysiologically based pharmacokinetic modeling of the lactating rat and nursing pup: A multiroute exposure model for trichloroethylene and its metabolite, trichloroacetic acidCited by: Trichloroethylene (Tri) metabolites, i.e.
chloral hydrate (Chl), trichloroethanol (TCE) and trichloroacetic acid (TCA), were administered to volunteers to determine the pharmacokinetic activity in the blood and urine. Immediate oxidation of Chl to TCA amounting to approx. 50% was followed by slow subsequent formation of TCA persisting for 30 by: Blood level kinetics of trichloroethylene and its metabolites confirmed a faster rate of metabolism in the mouse than in the rat.
Peak concentrations of the metabolites were reached within 2 hr of dosing in the mouse compared to 10 to 12 hr in the by: Metabolites derived from the GSH conjugate of TCE, in contrast, have been associated with the kidney as a target organ (Davidson and Beliles ; Lash, Fisher et al.
Dichlorovinylcysteine (DVC), in particular, is also mutagenic and may cause DNA damage in mammalian cells in vitro and in vivo (NTP ). Hathway DE () Consideration of the evidence for mechanisms of 1,1,2-trichloroethylene metabolism, including new identification of its dichloroacetic acid and trichloroacetic acid metabolites in mice.
Cancer Lett 8: – PubMed CrossRef Google ScholarCited by: Development of a Physiologically Based Pharmacokinetic Model of Trichloroethylene and Its Metabolites for Use in Risk Assessment.
(TCA), and dichloroacetic acid (DCA), in the mouse, rat. Physiologically based pharmacokinetic modeling with trichloroethylene and its metabolite, trichloroacetic acid, in the rat and mouse. Toxicol Appl Pharmacol Fisher JW, Mahle DA, Abbas R.
A human physiologically based pharmacokinetic model for trichloroethylene and its metabolites, trichloroacetic acid and free trichloroethanol. Title:A Review of Pharmacokinetic Parameters of Metabolites and Prodrugs VOLUME: 7 ISSUE: 2 Author(s):Michel Leandro de Campos, Elias Carvalho Padilha and Rosangela Goncalves Peccinini Affiliation:Sao Paulo State University – UNESP School of Pharmaceutical Sciences Rodovia Araraquara-Jau Km.
01 s/n, City: Araraquara, State: Sao Paulo, Zip code: ; Brazil. For example, blood concentrations of the three metabolites of trichloroethylene—chloral hydrate, trichloroethanol, and trichloroacetic acid— over time after administration of an oral dose of trichloroethylene at 1, mg/kg to male Osborne-Mendel rats and male B6C3F 1 mice were markedly higher in mice than in rats, whereas concentrations for trichloroethylene were higher in rats than in .As discussed in the mini-monograph article on trichloroethylene (TCE) pharmacokinetics (Chiu et al.
b), exposure to TCE results in a complex internal mixture of parent compound and its metabolites [see Chiu et al. (b) for a postulated metabolism scheme].Many of these metabolites have been shown to have toxicologic effects in TCE target organs, and several hypotheses have been put forth Cited by: A physiologically based pharmacokinetic (PBPK) model was developed which provides a comprehensive description of the kinetics of trichioroethylene (TCE) and its metabolites, trichioroethanol (TCOH), and trichloroacetic acid (TCA), in the mouse, rat, and human, for both oral and inhalation exposure.
The model includes descriptions of the three principal target tissues for cancer identified in Cited by: