Altered Retinoid Metabolism in Female Long-Evans and Han/Wistar Rats following Long-Term 2,3,7,8-Tetrachlorodibenzo-p-Dioxin (TCDD)-Treatment

Author:

Fletcher Nick,Giese Norbert,Schmidt Carsten,Stern Natalia,Lind P. Monica,Viluksela Matti,Tuomisto Jouni T.,Tuomisto Jouko,Nau Heinz,Håkansson Helen

Publisher

Oxford University Press (OUP)

Subject

Toxicology

Reference43 articles.

1. Abbott, B. D., and Birnbaum, L. S. (1989). Cellular alterations and enhanced induction of cleft palate after coadministration of retinoic acid and TCDD. Toxicol. Appl. Pharmacol.99,287–301.

2. Aust, S. D. (1984). On the mechanism of anorexia and toxicity of TCDD and related compounds. In Banbury Report 18. Biological Mechanisms of Dioxin Action (A. Poland and R. D. Kimbrough, Eds.), pp. 309–315, Cold Spring Harbour Laboratory, New York.

3. Balmer, J. E., and Blomhoff, R. (2002). Gene expression regulation by retinoic acid. J. Lipid Res.43,1773–1808.

4. Bastomsky, C. H. (1977). Enhanced thyroxine metabolism and high uptake goiters in rats after a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Endocrinology101,292–296.

5. Brouwer, A., Hakansson, H., Kukler, A., Van den Berg, K. J., and Ahlborg, U. G. (1989). Marked alterations in retinoid homeostasis of Sprague-Dawley rats induced by a single i.p. dose of 10 micrograms/kg of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Toxicology58,267–283.

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