Jörg Schuppler

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Numerous drugs, hormones and environmental pollutants induce liver growth by hypertrophy and/or hyperplasia, and promote preferential growth of putative preneoplastic foci in the liver. In the present study the regression of hyperplasia after cessation of inducer/promoter treatment was studied in normal liver and in liver foci. High doses of cyproterone(More)
Treatment of female Wistar rats with cyproterone acetate (CPA) leads to considerable enlargement of the liver. The organ content of water, dry mass, protein, RNA, and DNA increased in parallel with the enlargement; only lipid accumulation showed a slight excess. The changes were maximal after treatment for 3 days and increased in a dose-dependent manner,(More)
Putative preneoplastic foci (islands) of altered hepatocytes were induced by single doses of initiating hepatocarcinogens and identified by various histochemical and morphological markers. DNA synthesis, measured by 3H-thymidine and autoradiography, as well as mitotic activity were found to be higher in the foci than in normal hepatocytes. Without promotion(More)
According to the multistage concept of carcinogenesis, promoters induce selective or preferential multiplication of initiated cells, thereby accelerating one of the rate-limiting steps in cancer formation. The driving force for this selective growth of initiated cells is not known. In normal liver, various liver tumour promoters induce expression of(More)
Putative preneoplastic islands were induced in rat liver by diethylnitrosamine or nitrosomorpholine administered either as single high doses or continuously for 40 days at low dose levels. Following recovery periods of 3 weeks to 11 months, islands were identified by means of a positive gamma-glutamyl transferase reaction and/or altered morphology. DNA(More)
Endogenous (estradiol-17 beta; progesterone) and synthetic (ethinyl estradiol; cyproterone acetate; norethindrone acetate; norethynodrel) sex steroids were evaluated for tumor-initiating activity in the rat liver using the Solt-Farber system. All steroids were negative. This provides further evidence that tumor formation in long-term rodent bioassays by(More)
Putative preneoplastic foci of rat liver, so far believed to be deficient in monooxygenases, are shown to contain a cytochrome P450 isoenzyme inducible by phenobarbital. The isoenzyme is also present and appears catalytically active in liver tumors obtained after promotion with phenobarbital and alpha-hexachlorocyclohexane.
A number of different compounds, including phenobarbital, hypolipidemic drugs such as clofibrate and nafenopin, the sex steroids progesterone, cyproterone acetate, estradiol and mestranol, chlorinated hydrocarbons such as DDT, hexachlorocyclohexane, and TCDD and the antioxidant butylhydroxytoluene, appears to promote the development of liver tumors from(More)