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暴露于苯并(a)芘的金头鲷的组织病理学改变、EROD活性、CYP1A蛋白和胆汁代谢产物

Histopathological alterations, EROD activity, CYP1A protein and biliary metabolites in gilthead seabream Sparus aurata exposed to benzo(a)pyrene.

作者信息

Ortiz-Delgado J B, Segner H, Arellano J M, Sarasquete C

机构信息

Institute of Marine Sciences of Andalucía, CSIC, Polígono Río San Pedro, Puerto Real, Cádiz, Spain.

出版信息

Histol Histopathol. 2007 Apr;22(4):417-32. doi: 10.14670/HH-22.417.

DOI:10.14670/HH-22.417
PMID:17290352
Abstract

This study compared for seabream, Sparus aurata exposed to benzo(a)pyrene-B(a)P-, the response of molecular cytochrome P450 1A (CYP1A) and cellular histopathology biomarkers. Male gilthead seabream, Sparus aurata specimens were exposed for 20 days via water to a series of high B(a)P concentrations. CYP1A was assessed by measuring enzymatic activity (EROD) and CYP1A protein content, and cellular responses were evaluated by routine histopathological methods. In addition, biliary metabolites were measured in order to verify that B(a)P was absorbed and metabolised. Histological lesions, both in liver and gills, increased in parallel to B(a)P concentrations, with the majority of changes representing rather non-specific alterations. Hepatic EROD and CYP1A proteins data showed a concentration-dependent induction, while in the gills, EROD activity but not CYP1A proteins showed a non-monotonous dose response, with a maximum induction level at 200 microg B(a)P.L-1 and decreasing levels thereafter. The findings provide evidence that short-term, high dose exposure of fish can result in significant uptake and metabolism of the lipophilic B(a)P, and in pronounced pathological damage of absorptive epithelia and internal organs.

摘要

本研究比较了暴露于苯并(a)芘(B(a)P)的金头鲷(Sparus aurata)分子细胞色素P450 1A(CYP1A)和细胞组织病理学生物标志物的反应。雄性金头鲷标本通过水暴露于一系列高浓度的B(a)P中20天。通过测量酶活性(EROD)和CYP1A蛋白含量来评估CYP1A,并通过常规组织病理学方法评估细胞反应。此外,测量胆汁代谢物以验证B(a)P是否被吸收和代谢。肝脏和鳃的组织学损伤与B(a)P浓度平行增加,大多数变化表现为非特异性改变。肝脏EROD和CYP1A蛋白数据显示出浓度依赖性诱导,而在鳃中,EROD活性而非CYP1A蛋白表现出非单调剂量反应,在200μg B(a)P·L-1时诱导水平最高,此后水平下降。研究结果表明,鱼类短期高剂量暴露可导致亲脂性B(a)P的大量摄取和代谢,并对吸收上皮和内脏器官造成明显的病理损伤。

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