Brtko J, Filipcík P, Hudecová S, Brtková A, Bransová J
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Biol Trace Elem Res. 1998 Apr-May;62(1-2):43-50. doi: 10.1007/BF02820020.
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 RARalpha and the type I iodothyronine 5'-deiodinase gene expression in the GH4C1 rat pituitary tumor cells. SeIV at 1.0 micromol/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 micromol/L reduced (p < 0.05) the RA specific binding to RAR in liver, as well. Seleno-L-methionine (Se-II) when compared to L-methionine did not exert any inhibitory effect on the formation of the RA-RAR complex. SeIV (up to 2.5 micromol/L) has no inhibitory effect on GH4C1 cell proliferation as well as the prolactin secretion. SeIV at 1.0 micromol/L significantly decreases the rate of mRNA synthesis and/or degradation of the alpha 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 RARalpha, with the cell vitality and the cell growth remaining unchanged.
本研究旨在探讨亚硒酸盐（SeIV）和硒酸盐（SeVI）对大鼠肝脏中全反式维甲酸（RA）-核维甲酸受体（RAR）复合物形成的影响。我们还展示了关于SeIV对GH4C1大鼠垂体瘤细胞中RARα和I型碘甲状腺原氨酸5'-脱碘酶基因表达的体外影响的数据。发现1.0微摩尔/升的SeIV可降低（p<0.05）大鼠肝脏中RA与RAR的特异性结合。二硫苏糖醇（DTT），一种巯基保护剂，在受SeIV影响时对保护RAR结合特性略有效果。0.1微摩尔/升的SeVI也降低（p<0.05）了肝脏中RA与RAR的特异性结合。与L-甲硫氨酸相比，硒代-L-甲硫氨酸（Se-II）对RA-RAR复合物的形成没有任何抑制作用。SeIV（高达2.5微摩尔/升）对GH4C1细胞增殖以及催乳素分泌没有抑制作用。1.0微摩尔/升的SeIV显著降低RARα形式的mRNA合成和/或降解速率，并导致GH4C1细胞中I型碘甲状腺原氨酸5'-脱碘酶基因表达增强。基于体外实验的结果表明，无机硒可能影响RA与其同源受体分子的特异性结合，并可能降低编码RARα的基因的表达，而细胞活力和细胞生长保持不变。
