In vivo modulation of nonylphenol-induced zonagenesis and vitellogenesis by the antiestrogen, 3,3′4,4′-tetrachlorobiphenyl (PCB-77) in juvenile fish

In vivo modulation of nonylphenol-induced zonagenesis and vitellogenesis by the antiestrogen, 3,3′4,4′-tetrachlorobiphenyl (PCB-77) in juvenile fish
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DOI:
10.1016/s1382-6689(01)00063-1
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发表时间:
2001-05-01
影响因子:
4.3
通讯作者:
Goksoyr, A
Goksoyr, A
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Arukwe, A;Yadetie, F;Goksoyr, A

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卵带发生和卵黄发生(分别是蛋壳带辐射蛋白(Zrp)和卵黄原蛋白(Vtg)的产生)是卵生脊椎动物卵黄发生的两个雌激素调节过程,对卵母细胞成熟至关重要。在两个单独的实验中,壬基酚(NP; 25 mg kg(-1))单独或与3,3',4,4'-四氯联苯(TCB; 0.1 mg kg(-1))联合处理大西洋鲑幼鱼(Salmo salar)导致血浆蛋壳Zrp和Vtg及其各自的肝脏mRNA水平显著升高。单独TCB处理可引起CYP1A mRNA、蛋白和酶(7-乙氧基间苯二酚o -去乙基酶(EROD))水平升高。在实验3中,也包括时间因素,与单独NP处理相比,幼年鲑鱼暴露于每公斤10和25 mg NP与TCB联合处理通常会导致血浆Zrp和Vtg水平降低。在第四个实验中,幼年鲑鱼在单剂量NP (25 mg kg(-1))前两天或后两天暴露于不同剂量的TCB。NP暴露后5天采集样本,分析mRNA和蛋白质水平。一般来说,NP暴露后2天给予TCB剂量导致Vtg和Zrp蛋白和mRNA水平升高。Vtg和Zrp mRNA。在NP暴露前2天,0.1 mg TCB组的水平也有所升高。在所有实验中,TCB注射诱导肝脏CYP1A mRNA、CYP1A蛋白和EROD活性,但单独给药时未观察到Zrp或Vtg蛋白/mRNA的诱导。本研究首次记录了抗雌激素cyp1a诱导剂对鱼类或任何其他低等脊椎动物异种雌激素诱导反应的明显刺激。然而,TCB对NP诱导反应的刺激或抑制作用似乎取决于NP和TCB剂量的比例以及暴露的时间顺序。鱼类肝带生成和卵黄形成继续为进一步研究内分泌干扰物和cyp1a诱导剂之间的机制和可能的相互作用,以及它们的抗雌激素和/或雌激素增强作用提供了有趣的模型。(C) 2001 Elsevier Science B.V.版权所有
Zonagenesis and vitellogenesis (eggshell zona radiata protein (Zrp) and vitellogenin (Vtg) production, respectively), are two estrogen-regulated processes in oviparous vertebrates that are crucial for oocyte maturation. Treatment of juvenile Atlantic salmon (Salmo salar) with nonylphenol (NP; 25 mg kg(-1)) alone or in combination with 3,3',4,4'-tetrachlorobiphenyl (TCB; 0.1 mg kg(-1)) resulted in pronounced elevations of plasma eggshell Zrp and Vtg and their respective liver mRNA levels in two separate experiments. TCB treatment alone caused the elevation of CYP1A mRNA, protein and enzyme levels (7-ethoxyresorufin O-deethylase (EROD)). In experiment 3, which also included the time factor, exposure of juvenile salmon to 10 and 25 mg NP per kg in combination with TCB generally resulted in reduced plasma Zrp and Vtg levels, compared with NP treatments alone. In a fourth experiment, juvenile salmon were exposed to different doses of TCB either 2 days before or 2 days after a single dose (25 mg kg(-1)) of NP. Samples were always collected 5 days after the NP exposure and analyzed for mRNA and protein levels. Generally, TCB doses given 2 days after NP exposure resulted in the elevation of Vtg and Zrp protein and mRNA levels. Vtg and Zrp mRNA. levels were also elevated in the groups treated with 0.1 mg TCB 2 days before NP exposure. In all experiments, TCB injection resulted in the induction of liver CYP1A mRNA, CYP1A protein and EROD activity: but no Zrp or Vtg protein/mRNA inductions were observed when given alone. The present study documents for the first time the apparent stimulation of xenoestrogen-induced responses by an antiestrogenic CYP1A-inducer, in fish or any other lower vertebrate. However, the stimulatory or inhibitory effect of TCB on NP-induced responses appear to be dependent on the ratio of NP and TCB doses, and temporal sequence of exposure. Fish hepatic zonagenesis and vitellogenesis continue to provide interesting models for further studies on the mechanisms and possible interactions between endocrine disrupters and CYP1A-inducers, their antiestrogenic and/or estrogen potentiating effects. (C) 2001 Elsevier Science B.V. All rights reserved.