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首页> 外文期刊>Life sciences >Species-specific induction of CYP2B by 2,4,6-tryphenyldioxane-1,3 (TPD).
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Species-specific induction of CYP2B by 2,4,6-tryphenyldioxane-1,3 (TPD).

机译：CYP2b的特异性诱导2,4,6- rotephenyldioxane-1,3（TPD）。

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AIM: The aim of the current study was to investigate the species-specific induction of CYP2B by 2,4,6-tryphenyldioxane-1,3 (TPD) in relation to activation of CAR. MAIN METHODS: 7-Pentoxyresorufin O-dealkylase (PROD) activity, RT-PCR, Western blot, Electrophoretic mobility shift assays (EMSA). KEY FINDINGS: Phenobarbital-like inducer administration significantly up-regulated CYP2B activity in rat and mouse liver in a species-specific manner, in contrast to the effects on CYP2B in lungs, kidneys and brains. In parallel, Western blot analysis showed that the species-specific increase of PROD in liver is related to the high content of CYP2B: phenobarbital (PB) and TPD increased CYP2B in rat liver, PB and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP) - in mouse liver. The CYP2B protein level was unchanged in the lungs of rats and mice after inducer treatment, whereas it was not detected in the kidney and brain of control and treated animals. The hepatic CYP2B activity in both species paralleled the increase of CYP2B mRNA. A detectable CYP2B mRNA level was measured in the lungs of untreated mice and rats, though it was unchanged during induction. Noninducibility of CYP2B in extrahepatic tissues accompanied an absence of constitutive androstane receptor (CAR) gene expression in these tissues. In liver CYP2B induction paralleled the high level of CAR expression detected by RT-PCR. Moreover, PB, TPD and TCPOBOP treatment stimulated nuclear accumulation of CAR and increased CAR receptor NR1-binding activity in animal liver in a species-specific manner. SIGNIFICANCE: We have shown that the increased nuclear accumulation and binding activity of CAR are associated with the species-specific up-regulation of CYP2B by TPD in rat liver.
机译：目的：本研究的目的是通过相对于CAR的活化2,4,6- tryphenyldioxane -1,3（TPD）调查CYP2B的物种特异性诱导。主要方法：7- Pentoxyresorufin O型脱烷基（PROD）活性，RT-PCR，蛋白质印迹，电泳迁移率变动分析（EMSA）。主要调查结果：苯巴比妥样的物种特异性的方式在大鼠和小鼠肝脏诱导管理显著上调的CYP2B活性，而相比之下，在肺，肾和大脑对CYP2B的影响。平行地，Western印迹分析显示，在肝PROD的物种特异性增加与CYP2B的高含量：苯巴比妥（PB）和TPD大鼠肝脏增加CYP2B，PB和1,4-双[2-（3- ，5- dichloropyridyloxy）]苯（TCPOBOP） - 小鼠肝脏。该CYP2B蛋白水平在诱导治疗后，大鼠和小鼠的肺不变，而这是不是在控制和治疗动物的肾脏和大脑检测。在这两个物种的肝CYP2B活性平行CYP2B mRNA的增加。可检测CYP2B mRNA水平在未处理的小鼠和大鼠的肺中测量的，虽然它是诱导过程中保持不变。在肝外组织CYP2B不能诱发伴有不存在在这些组织中组成型雄烷受体（CAR）的基因表达的。在肝脏CYP2B感应平行通过RT-PCR检测到的CAR表达的高水平。此外，PB，TPD和TCPOBOP治疗刺激CAR的核积累和增加CAR受体物种特异的方式NR1结合在动物肝脏活动。意义：我们已经表明，增加的核积累和CAR的结合活性与物种特异性上调CYP2B由TPD大鼠肝脏相关。

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