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© 1990 Oxford University Press

research-article

Effect of chemical carcinogens on cholesterol biosynthetic pathways in the skin of mice

Yutaka Tanimoto, Ken-ichi Fukao, Koji Yoshiga, Kazuaki Takada, Yoshihiko Ohyama and Kyuichiro Okuda

Department of Oral and Maxillofacial Surgery I and Department of Biochemistry, Hiroshima University, School of Dentisuy Hiroshima 734, Japan

The metabolism of zymosterol and mevalonic acid was studied in vitro using the skin homogenates of 3-methylcholanthrene (3MC), diazachotesterol-treated and untreated mice. In normal mouse skin only lathosterol was a major metabohte and the other metabolites, cholesta-5,7,24-trien-3ß-ol, desmosterol, cholesterol and 7-dehydrocholesterol were much less abundant. However, in the skin homogenate of mice treated with 3MC lathosterot production was depressed, while the production of cholesta-5,7,24-tiien-3ß-ol and desmosterol was significantly increased, the cholesterol levelbeing normal or a little higher. In contrast, in the skin homogenate of mice administered diazacholesterol the production of both lathosterol and cholesterol was almost completely blocked with the slightly increased production of cholesta-5,7,24-trien-3ß-ol and desmosterol. The metabolism in vitro of [2–14C]-mevalonic acidwas quite similar to that of zymosterol, and no additional product which might possibly have been produced by the Kandutsch-Russell pathway was observed. Two pathways for cholesterol biosynthesis, therefore, may exist in mouse skin; the first is lanosterol -> zymosterol -> 5{alpha}-cholesta-7,24-dien-3ß-ol -> lathosterol -> 7-dehydro-cholesterol -> cholesterol, and the second by Bloch: lanosterol -> zymosterol -> 5{alpha}-cholesta-7,24-dien-3ß-ol -> cholesta 5,7,24-trien-3ß-ol -> desmosterol -> cholesterol. When moose skin is treated with 3-MC the former pathway is virtually blocked and the latter is stimulated, keeping the level of cholesterol in the tissue constant or a little higher than normal, which seems to be a significant change in the early stage of chemical carcinogenesis.


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