Nuclear all-trans retinoic acid receptors |
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Authors: | Julius Brtko Peter Filipčík Soňa Hudecová Anastázia Brtková Janette Bransová |
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Institution: | (1) Institute of Experimental Endocrinology, Slovak Academy of Sciences, 833 06 Bratislava, Slovak Republic;(2) Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences, 833 34 Bratislava, Slovak Republic;(3) Research Institute of Nutrition, 833 37 Bratislava, Slovak Republic |
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Abstract: | The present study was undertaken to investigate the effects of selenite (SeIV) and selenate (SeVI) on the all-trans retinoic acid (RA)-nuclear retinoic acid receptor (RAR) complex formation in rat liver. We also present
the data on the in vitro effects of SeIV on the RARα and the type I iodothyronine 5′-deiodinase gene expression in the GH4C1 rat pituitary tumor cells. SeIV at 1.0 μmol/L was found to reduce (p<0.05) the RA specific binding to RAR in rat liver. Dithiothreitol (DTT), a protective agent for sulfhydryl groups, was found
to be slightly effective in protecting the RAR binding properties when affected by SeIV. SeVI at 0.1 μmol/L reduced (p<0.05) the RA specific binding to RAR in liver, as well. Seleno-l-methionine (Se-II) when compared tol-methionine did not exert any inhibitory effect on the formation of the RA-RAR complex. SeIV (up to 2.5 μmol/L) has no inhibitory effect on GH4C1 cell proliferation as well as the prolactin secretion. SeIV at 1.0 μmol/L significantly decreases the rate of mRNA synthesis and/or degradation of the α form of the RAR and causes the
enhancement of the type I iodothyronine 5′-deiodinase gene expression in GH4C1 cells.
The results based on in vitro experiments suggest that inorganic selenium may affect the RA specific binding to their cognate
receptor molecules, and it may reduce expression of the gene encoding the RARα, with the cell vitality and the cell growth
remaining unchanged. |
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Keywords: | All-trans retinoic acid nuclear retinoic acid receptor selenium iodothyronine 5′ -deiodinase rat liver GH4C1 pituitary tumor cells nuclear receptor gene expression |
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