The metabolism of 36Cl-labelled trichloroethylene and tetrachloroethylene in the rat

Daniel, J.W.

doi:10.1016/0006-2952(63)90109-6

Cited by 133 publications

(44 citation statements)

References 12 publications

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“…In fact, the half-life of TCE in adipose tissue is estimated to be 3.5-5 hr, whereas that in both the richly and poorly perfused compartments is estimated to be 2-4 min (4 Daniel (12) dosed rats by stomach tube (60 mg/kg) with labeled TCE and reported that 90-95% of the radiolabel was recovered in expired air and urine. Dekant et al (13) gavage-dosed mice and rats with 200 mg/kg of labeled TCE in corn oil and recovered 93-98% of the radiolabel.…”

mentioning

confidence: 99%

Metabolism of trichloroethylene.

Lash

Fisher

Lipscomb

et al. 2000

Environ Health Perspect

250

246

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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-dependent differences in biotransformation pathways. Defining these differences can play an important role in the utility of laboratory animal data for understanding the pharmacokinetics and pharmacodynamics of TCE in humans. Sex-, species-, and strain-dependent differences in absorption and distribution of TCE may play some role in explaining differences in metabolism and susceptibility to toxicity from TCE exposure. The majority of differences in susceptibility, however, are likely due to sex-, species-, and strain-dependent differences in activities of the various enzymes that can metabolize TCE and its subsequent metabolites. An additional factor that plays a role in human health risk assessment for TCE is the high degree of variability in the activity of certain enzymes. TCE undergoes metabolism by two major pathways, cytochrome P450 (P450)-dependent oxidation and conjugation with glutathione (GSH). Key P450-derived metabolites of TCE that have been associated with specific target organs, such as the liver and lungs, include chloral hydrate, trichloroacetate, and dichloroacetate. Metabolites derived from the GSH conjugate of TCE, in contrast, have been associated with the kidney as a target organ. Specifically, metabolism of the cysteine conjugate of TCE by the cysteine conjugate ,B Iyase generates a reactive metabolite that is nephrotoxic and may be nephrocarcinogenic. Although the P450 pathway is a higher activity and higher affinity pathway than the GSH conjugation pathway, one should not automatically conclude that the latter pathway is only important at very high doses. A synthesis of this information is then presented to assess how experimental data, from either animals or from in vitro studies, can be extrapolated to humans for risk assessment.

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mentioning

confidence: 99%

Metabolism of trichloroethylene.

Lash

Fisher

Lipscomb

et al. 2000

Environ Health Perspect

250

246

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“…In the liver, however, tetrachloroethylene is thought to bc oxidized by cytochrome P-450-catalyzed monooxygenases to an epoxide, which undergoes an intramolecular rearrangement to trichloroacetylchloride, followed by conversion to trichloroacetic acid [111][112][113][114]. There are no obvious reasons why such a mechanism could not operate in microbial systems too.…”

Section: Aerobic Degradation Of Chlorinated Ethylenesmentioning

confidence: 99%

Degradation of halogenated aliphatic compounds: The role of adaptation

Pries

1994

FEMS Microbiology Reviews

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A limited number of halogenated aliphatic compounds can serve as a growth substrate for aerobic microorganisms. Such cultures have (specifically) developed a variety of enzyme systems to degrade these compounds. Dehalogenations are of critical importance. Various heavily chlorinated compounds are not easily biodegraded, although there are no obvious biochemical or thermodynamic reasons why microorganisms should not be able to grow with any halogenated compound. The very diversity of catabolic enzymes present in cultures that degrade halogenated aliphatics and the occurrence of molecular mechanisms for genetic adaptation serve as good starting points for the evolution of catabolic pathways for compounds that are currently still resistant to biodegradation.

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“…Per wird überwiegend unverändert von Ratte [21,22], Maus [23] und Mensch [19,24] abgeatmet. Nur ein sehr geringer Anteil wird metabolisiert [22�24].…”

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“…Nur ein sehr geringer Anteil wird metabolisiert [22�24]. Für den Umsatz wird folgender Weg angenommen [22,23,25]:…”

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Tetrachlorethylen H [MAK Value Documentation in German language, 1974]

2012

The MAK‐Collection for Occupational Health and Safety

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Veröffentlicht in der Reihe Gesundheitsschädliche Arbeitsstoffe , 3. Lieferung, Ausgabe 1974 Der Artikel enthält folgende Kapitel: Allgemeiner Wirkungscharakter Erfahrungen beim Menschen Tierexperimentelle Befunde Inhalation Andere Applikationsarten Begründung des MAK‐Wertes

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The metabolism of 36Cl-labelled trichloroethylene and tetrachloroethylene in the rat

Cited by 133 publications

References 12 publications

Metabolism of trichloroethylene.

Metabolism of trichloroethylene.

Degradation of halogenated aliphatic compounds: The role of adaptation

Tetrachlorethylen H [MAK Value Documentation in German language, 1974]

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