F
Franz Oesch
Researcher at University of Mainz
Publications - 580
Citations - 22320
Franz Oesch is an academic researcher from University of Mainz. The author has contributed to research in topics: Epoxide hydrolase & Microsomal epoxide hydrolase. The author has an hindex of 76, co-authored 578 publications receiving 21684 citations. Previous affiliations of Franz Oesch include University of Basel & National Institutes of Health.
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Journal Article
Aryl hydrocarbon hydroxylase, epoxide hydrase, and 7,12-dimethylbenz(a)anthracene-produced skin tumorigenesis in the mouse.
TL;DR: Mouse skin tumorigenesis initiated by 7,12-dimethylbenz[ a ]anthracene and promoted by repeated applications of phorbol ester is unrelated to genetic diffrences in the extent of aryl hydrocarbon hydroxylase induction by polycyclic hydrocarbons in inbred or hybrid C57BL/6N and DBA/2N mice.
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A reconstituted microsomal enzyme system that converts naphthalene to trans-1,2-dihydroxy-1,2-dihydronaphthalene via naphthalene-1,2-oxide: presence of epoxide hydrase in cytochrome P-450 and P-448 fractions.
TL;DR: Cytochrome P -450 and P -448 fractions isolated from rat liver microsomes contain high levels of epoxide hydrase activity with styrene oxide or naphthalene-1,2-oxide as substrate, and its conversion to dihydrodiol can be blocked by the epoxidehydrase inhibitor, 3,3,3-trichloropropene oxide.
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Distribution and inducibility of cytosolic epoxide hydrolase in male sprague-dawley rats
TL;DR: Cytosolic epoxide hydrolase activity was present in all of six extrahepatic rat tissues investigated and specific activities were very high in the heart and kidney, followed by liver greater than brain greater than lung greater than testis greater than spleen.
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Styrene metabolism, genotoxicity, and potential carcinogenicity.
Pavel Vodicka,Mikko Koskinen,Alessio Naccarati,Barbara Oesch-Bartlomowicz,Ludmila Vodickova,Kari Hemminki,Franz Oesch +6 more
TL;DR: Individual susceptibility depending on metabolism polymorphisms and individual DNA repair capacity as well as the dependence of the nonlinearity of the dose-response relationships in the species in question and the consequences for risk evaluation are analyzd.
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Prevention of benzo(a)pyrene-induced mutagenicity by homogeneous epoxide hydratase.
TL;DR: It is demonstrated that the metabolic pathway responsible for the mutagenicity of both polycyclic hydrocarbons observed in this system proceeds entirely via an epoxidation pathway and that the responsible metabolites are epoxides or species arising from them.