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Receptors and Other Targets for Toxic Substances - Proceedings of the European Society of Toxicology, Meeting Held in Budapest, June 11-14, 1984 (Paperback, Softcover reprint of the original 1st ed. 1985)
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Receptors and Other Targets for Toxic Substances - Proceedings of the European Society of Toxicology, Meeting Held in Budapest, June 11-14, 1984 (Paperback, Softcover reprint of the original 1st ed. 1985)
Series: Archives of Toxicology, 8
Expected to ship within 10 - 15 working days
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Trichloroethylene (TRI), administered orally at high doses for 18
months has been shown to increase the incidence of hepatocellular
carcinoma in B6C3F 1 mice but not Osborne-Mendel rats (NCI, 1976).
The interpretation of these studies has been confounded due to the
presence of epoxide stabilizers in the TRI. However more recent
studies have demonstrated that pure TRI also causes hepatocellular
carcinoma in B6C3F mice (NTP, 1983) and Aldedey Park (Swiss) mice
(Elcombe 1 and Pratt, unpublished data). Furthermore, no increase
in the incidence of hepatocellular carcinoma was observed in Fisher
344 rats administered pure TRI (NTP, 1983). TRI has been
extensively examined for mutagenic potential, but many studies were
bedeviled by the presence of mutagenic epoxide stabilizers.
However, in general, TRI has been found to be only 'marginally'
mutagenic or non-mutagenic (Greim et ai., 1975; Simmon et ai.,
1977; Bronzetti et ai., 1978; Waskell, 1978; Bartsch et ai., 1979;
Slacik-Erben et ai., 1980). Covalent binding of trichloroethylene
or its metabolites to protein, RNA and DNA has been illustrated in
vitro (Van Duuren and Banerjee, 1976; Bolt et ai., 1977; Bolt and
Filser, 1977; Uehleke and Poplawski-Tabarelli, 1977; Banerjee and
Van Dauren, 1978). However, in vivo, only extremely low
(indistinguishable from protein binding) or zero binding of TRI
metabolites to DNA has been reported (Parchman and Magee, 1982;
Stott et ai., 1982).
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