Retinoid status and responsiveness to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice lacking retinoid binding protein or retinoid receptor forms

P. Hoegberg, C.K. Schmidt, N. Fletcher, C.B. Nilsson, C. Trossvik, A. Gerlienke Schuur, A. Brouwer, H. Nau, N.B. Ghyselinck, P Chambon, H. Hakansson

Research output: Contribution to JournalArticleAcademicpeer-review

Abstract

We have investigated the role of Vitamin A (retinoid) proteins in hepatic retinoid processing under normal conditions and during chemical stress induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a chemical known to interfere with retinoid turnover and metabolism. Three separate studies were performed in wildtype control mice and transgenic mice that lack one or more isoforms of retinoic acid receptors (RAR), retinoid X receptors (RXR), or intracellular retinoid-binding proteins (CRABP I, CRABP II, CRBP I). Body and organ weight development was monitored from 2 weeks of age to adult, and hepatic levels of retinyl esters, retinol, and retinoic acid were investigated. In addition, hepatic concentrations of 9-cis-4-oxo-13,14-dihydro-retinoic acid, a recently discovered retinoid metabolite that has proven sensitive to both TCDD exposure and Vitamin A status, were also determined. Mice absent in the three proteins CRBP I, CRABP I, and CRABP II (CI/CAI/CAII
Original languageEnglish
Pages (from-to)25-39
Number of pages15
JournalChemico-Biological Interactions
Volume156
Issue number1
DOIs
Publication statusPublished - 2005

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