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首页> 外文期刊>Environmental toxicology and chemistry >EXPRESSION AND INDUCIBILITY OF ARYL HYDROCARBON RECEPTOR PATHWAY GENES IN WILD-CAUGHT KILLIFISH (FUNDULUS HETEROCLITUS) WITH DIFFERENT CONTAMINANT-EXPOSURE HISTORIES
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EXPRESSION AND INDUCIBILITY OF ARYL HYDROCARBON RECEPTOR PATHWAY GENES IN WILD-CAUGHT KILLIFISH (FUNDULUS HETEROCLITUS) WITH DIFFERENT CONTAMINANT-EXPOSURE HISTORIES

机译：具有不同污染物暴露历史的野生硬藻杀害动物（芳基异菌）中芳烃受体通路基因的表达和诱导性

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Wildcaught killifish from a contaminated site on the Elizabeth River (VA, USA) are refractory to induction of cytochrome P4501A (CYP1A, measured as catalytic activity and immunodetectable CYP1A protein) after exposure to typical aryl hydrocarbon receptor (AHR) agonists, as has been reported for fish from other sites highly contaminated with these compounds. In an attempt to understand the molecular basis for the lack of inducibility of CYP1A protein expression and activity in Elizabeth River killifish, we analyzed the expression of CYP1A and four other members of the AHR signal transduction pathway: AHR1, AHR2, AHR repressor (AHRR), and AHR nuclear translocator (ARNT). Gene expression was measured by cycle-optimized reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of messenger ribonucleic acid (mRNA) extracted from livers of killifish from the Elizabeth River and King's Creek (VA, USA) (reference site), 36 h after injection with β-naphthoflavone (BNF, an AHR agonist) or corn oil (carrier control). Hepatic CYP1A mRNA was inducible in King's Creek killifish. However, in Elizabeth River killifish, no induction of CYP1A mRNA was observed, confirming and extending previous results showing no induction of CYP1A protein or catalytic activity in this population. Similarly, AHRR and AHR2 mRNA levels were induced by BNF in King's Creek but not Elizabeth River killifish. No population or treatment-related differences were observed in expression of AHR1 or ARNT mRNAs. The results reveal in Elizabeth River killifish a consistent lack of inducibility of genes that are normally inducible by AHR agonists (CYP1A, AHRR, AHR2). However, the expression of AHR1, AHR2, and AHRR in vehicle-treated fish did not differ between Elizabeth River and King's Creek killifish, suggesting that altered constitutive expression of AHRs or AHRR does not underlie the refractory CYP1A phenotype in Elizabeth River killifish.
机译：据报道，来自伊丽莎白河（美国弗吉尼亚州）受污染地点的野生捕捞i鱼在暴露于典型的芳烃受体（AHR）激动剂后难以诱导细胞色素P4501A（CYP1A，以催化活性和可检测的CYP1A蛋白测量）。用于来自被这些化合物高度污染的其他地点的鱼。为了了解缺乏CYP1A蛋白表达和伊丽莎白河致死鱼诱导性的分子基础，我们分析了CYP1A和AHR信号转导途径的其他四个成员的表达：AHR1，AHR2，AHR阻遏物（AHRR） ，以及AHR核移位器（ARNT）。通过循环优化逆转录酶-聚合酶链反应（RT-PCR）分析基因表达来测量，信使核糖核酸（mRNA）是从伊丽莎白河和金斯克里克（美国弗吉尼亚州）的kill鱼肝脏中提取的（参考位点），36注射β-萘黄酮（BNF，一种AHR激动剂）或玉米油（载体对照）后h。肝CYP1A mRNA在King's Creek i鱼中可诱导。然而，在伊丽莎白河的河豚鱼中，未观察到CYP1A mRNA的诱导，证实并扩展了先前的结果，表明该人群中未诱导CYP1A蛋白或催化活性。同样，AHNF和AHR2 mRNA水平是由BNF诱导的在King's Creek而不是伊丽莎白河的kill鱼中诱导的。在AHR1或ARNT mRNA的表达中未观察到任何与人群或治疗相关的差异。结果表明，伊丽莎白河河鱼类始终缺乏可被AHR激动剂（CYP1A，AHRR，AHR2）诱导的基因的诱导能力。然而，媒介处理过的鱼中AHR1，AHR2和AHRR的表达在伊丽莎白河和King's Creek鱼类之间没有差异，这表明AHRs或AHRR的组成型表达的改变并不构成伊丽莎白河鱼类的难治性CYP1A表型的基础。

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