首页> 外文期刊>Comparative biochemistry and physiology, Part A. Molecular and integrative physiology >Transient inhibition of cyp1a gene transcription and EROD activity by musk xylene exposure in two fish cell lines PLHC-1 and RTG-2
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Transient inhibition of cyp1a gene transcription and EROD activity by musk xylene exposure in two fish cell lines PLHC-1 and RTG-2

机译:麝香二甲苯暴露对两种鱼细胞系PLHC-1和RTG-2的cyp1a基因转录和EROD活性的瞬时抑制

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Musk xylene (MX) is one of the most used synthetic nitromusk fragrance in personal care products. The high release in the aquatic environment together with the evidence of bioaccumulation in aquatic organisms suggest that this chemical could be an actual concern for toxicological consequences. Nevertheless no much data are available on cellular pathways and mechanisms of toxicity in aquatic organisms. The aim of the present study was to investigate the capability of MX to interfere with phase I of biotransformation by looking at cyp1a gene transcription and related enzyme activity in two fish cell lines as PLHC-1 and RTG-2. A dose-dependent (2, 4, 20 μM) and time-dependent (6, 12 and 24 h) exposure experiments have been performed testing MX alone and combined with a known CYP1A inducer as B(a)P. A transient inhibition of cyp1a gene transcription was observed after 6 h in both cell lines which seems to recover dose-dependently after 24 in RTG-2 and less markedly in PLHC-1. EROD activity did not show clear effect after 6 h while resulted significantly inhibited in both cell lines after 24 h. A common pathway of inhibition at gene level could be thus hypothesised in both cell lines after 6 h of exposure confirmed by EROD activity inhibition at 24 h. The potential involvement of MX metabolites in cyp1a gene recovery after 24 h of exposure could be hypothesized. Results of the time dependent experiment also suggest a different pathway of gene regulation for MX compared to B(a)P.
机译:麝香二甲苯(MX)是个人护理产品中最常用的合成硝基麝香香料之一。在水生环境中的高释放以及在水生生物中生物蓄积的证据表明,该化学物质可能是毒理学后果的实际关注点。然而,关于水生生物的细胞途径和毒性机理尚无大量数据。本研究的目的是通过观察两个鱼类细胞系PLHC-1和RTG-2中的cyp1a基因转录和相关的酶活性,来研究MX干扰生物转化的I期的能力。已进行了剂量依赖性(2、4、20μM)和时间依赖性(6、12和24 h)暴露实验,单独测试MX并与已知的CYP1A诱导剂B(a)P组合使用。在两个细胞系中均在6小时后观察到cyp1a基因转录的短暂抑制,这似乎在RTG-2中在剂量依赖性恢复后于24小时出现,而在PLHC-1中则不明显。 EROD活性在6小时后没有显示出明显的作用,而导致在24小时后在两种细胞系中均被显着抑制。因此,可以通过暴露24小时内EROD活性的抑制,在两种细胞系中假设在基因水平上存在抑制作用的常见途径。可以假设24小时后MX代谢物可能与cyp1a基因的恢复有关。时间依赖性实验的结果还表明,与B(a)P相比,MX的基因调控途径不同。

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