Ah receptor and ARNT protein and mRNA concentrations in rat prostate: effects of stage of development and 2,3,7, 8-tetrachlorodibenzo-p-dioxin treatment.
Ah receptor and ARNT protein and mRNA concentrations in rat prostate: effects of stage of development and 2,3,7, 8-tetrachlorodibenzo-p-dioxin treatment.
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DOI：
10.1006/taap.1998.8597
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发表时间：
1999-03
影响因子：
3.8
通讯作者：
R. J. Sommer;K. M. Sojka;R. Pollenz;P. Cooke;R. Peterson
中科院分区：
文献类型：
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作者：
R. J. Sommer;K. M. Sojka;R. Pollenz;P. Cooke;R. Peterson
研究了发育阶段和2，3，7，8-四氯二苯并-对二恶英(TCDD)暴露对雄性大鼠生殖器官芳香烃受体(AhR)及其核转位蛋白(ArnT)含量的影响。发育中的大鼠前列腺腹侧和背外侧的AHR蛋白水平随着年龄的增长而下降，在出生后第1天到第21天之间下降了大约70%。前列腺背外侧的ARNT蛋白水平也随着年龄的增长而降低，但腹侧不随年龄的增长而降低。前列腺AhR和Arnt蛋白表达的发育性下降与AhR和Arnt基因表达的下降有关。孕16、18、20天胎鼠泌尿生殖窦AHR和Arnt蛋白含量与PND 7d时腹侧前列腺相似。成年雄性大鼠暴露于TCDD(0.2、1、5或25微克/kg，24 h)后，前列腺腹侧、背外侧、输精管和附睾区AhR减少，Arnt蛋白无明显变化。宫内和哺乳期暴露TCDD(1.0微克/kg丹参酮，GD15)不改变Arnt水平，但降低PND7的前列腺AhR蛋白水平，延缓前列腺腹侧和背侧AhR蛋白的发育性下降。TCDD(5微克/kg ip)处理仔鼠2 4h后，PND7上的AHR蛋白表达下调，而PND1上的AHR蛋白表达无明显变化。因此，随着年龄的增长，AHR和Arnt蛋白及mRNA的表达水平受到调节，而TCDD暴露只改变AHR蛋白的浓度。由于宫内和哺乳期接触TCDD只会降低PND 7的前列腺AhR，因此围产期TCDD暴露损害前列腺发育的机制不太可能是AhR下调。
Effects of stage of development and 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) exposure on aryl hydrocarbon receptor (AhR) and AhR nuclear translocator (ARNT) protein concentrations in reproductive organs of male rats were determined. AhR protein levels in developing rat ventral and dorsolateral prostate decreased with age, declining approximately 70% between Postnatal Days (PND) 1 and 21. ARNT protein levels also decreased with age in dorsolateral, but not ventral prostate. The developmental decreases in prostatic AhR and ARNT protein were associated with decreases in AhR and ARNT mRNA. AhR and ARNT protein concentrations in fetal urogenital sinus on Gestation Days (GD) 16, 18, and 20 were similar to levels in ventral prostate on PND 7. TCDD exposure of adult male rats (0.2, 1, 5, or 25 micrograms/kg po, 24 h) decreased AhR but not ARNT protein in ventral and dorsolateral prostate, vas deferens, and epididymis. In utero and lactational TCDD exposure (1.0 micrograms/kg dam po, GD 15) did not alter ARNT levels but reduced prostatic AhR protein levels on PND 7 and delayed the developmental decrease in AhR protein in ventral and dorsolateral prostate. Finally, pretreatment of rat pups for 24 h with TCDD (5 micrograms/kg ip) down-regulated prostatic AhR protein on PND 7, but not on PND 1. Thus, prostatic AhR and ARNT protein and mRNA levels are regulated with age, whereas only AhR protein concentration is altered by TCDD exposure. Because in utero and lactational TCDD exposure only decreased prostatic AhR on PND 7, it is unlikely that down-regulation of AhR is the mechanism by which perinatal TCDD exposure impairs prostate development.