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Interaction on biomarkers in goldfish after co-exposure to 17β-estradiol and benzo(a)pyrene

机译:在联合暴露于17β-雌二醇和苯并(a)芘后,金鱼中生物标志物的相互作用

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The aquatic environment is challenged with complex mixtures of pollutants, which may produce synergistic or antagonistic effects in organisms, interacting on the established biomarkers. This study focuses on the interaction on biomarker responses in male goldfish (Carassius auratus) after co-exposure to 17β-estradiol (E2) and benzo(a)pyrene (BaP). Vitellogenin (Vtg), endogenous E2 and ethoxyresorufin-O-deethylase (EROD) were examined to assess the estrogenic effect, steroidogenesis, and metabolism capacity. Exposure to E2 or BaP alone significantly induced the production of Vtg and EROD, respectively. However, these inductions were markedly depressed by the co-exposed chemical, indicative of a reciprocal inhibiting interaction on Vtg and EROD. In addition, the E2-induced steroidogenesis were also suppressed by the coexisting BaP, while the steroidogenesis were not affected by BaP alone. Therefore, our results support a reciprocal inhibiting interaction on the established biomarkers on the estrogenic effect and metabolism capacity, and a one-way inhibition on the steroidogenesis pathway in goldfish after co-exposure to E2 and BaP.
机译:水生环境受到复杂污染物混合物的挑战,这可能在生物体中产生协同或拮抗作用,在已建立的生物标志物上相互作用。本研究重点介绍在17β-雌二醇(E2)和苯并(A)芘(BAP)之后雄性金鱼(Carassius auratus)在雄性金鱼(Carassius auratus)中的生物标志物反应的相互作用。研究了vitellogenin(VTG),内源E2和乙醇乙烯磺酰基-O-脱甲基酶(EROD),以评估雌激素效果,甾体化和代谢能力。单独接触E2或BAP分别显着诱导VTG和EROD的产生。然而,通过共同暴露的化学物质显着抑制了这些诱导,这表明对VTG和EROD的互易抑制相互作用。此外,E2诱导的甾体过素也受到共存的抑制作用,而共发生的同时也不受到单独的烤盘的影响。因此,我们的结果支持对培养的生物标志物对雌激素效应和代谢能力的互易抑制相互作用,以及在连通到E2和BAP之后金鱼中的甾体化途径的单向抑制。

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