Strobel Anneli, Lille-Langøy Roger, Segner Helmut, Burkhardt-Holm Patricia, Goksøyr Anders, Karlsen Odd André
Alfred Wegener Institute Helmholtz Centre for Polar and Marine Research, Am Handelshafen 12, 27570 Bremerhaven, Germany.
Department of Biological Sciences, University of Bergen, Thormøhlensgate 53B, 5006 Bergen, Norway.
Polar Biol. 2022;45(2):345-358. doi: 10.1007/s00300-021-02992-4. Epub 2021 Dec 26.
The Antarctic ecosystem is progressively exposed to anthropogenic contaminants, such as polycyclic aromatic hydrocarbons (PAHs). So far, it is largely unknown if PAHs leave a mark in the physiology of high-Antarctic fish. We approached this issue via two avenues: first, we examined the functional response of the aryl hydrocarbon receptor (Ahr), which is a molecular initiating event of many toxic effects of PAHs in biota. and served as representatives for high-Antarctic Notothenioids, and Atlantic cod, as non-polar reference species. We sequenced and cloned the Ahr ligand binding domain (LBD) of the Notothenioids and deployed a GAL4-based luciferase reporter gene assay expressing the Ahr LBD. Benzo[]pyrene (BaP), beta-naphthoflavone and chrysene were used as ligands for the reporter gene assay. Second, we investigated the energetic costs of Ahr activation in isolated liver cells of the Notothenioids during acute, non-cytotoxic BaP exposure. In the reporter assay, the Ahr LBD of Atlantic cod and the Antarctic Notothenioids were activated by the ligands tested herein. In the in vitro assays with isolated liver cells of high-Antarctic Notothenioids, BaP exposure had no effect on overall respiration, but caused shifts in the respiration dedicated to protein synthesis. Thus, our study demonstrated that high-Antarctic fish possess a functional Ahr that can be ligand-activated in a concentration-dependent manner by environmental contaminants. This is associated with altered cost for cellular protein synthesis. Future studies have to show if the toxicant-induced activation of the Ahr pathway may lead to altered organism performance of Antarctic fish.
The online version contains supplementary material available at 10.1007/s00300-021-02992-4.
南极生态系统正逐渐受到人为污染物的影响,例如多环芳烃(PAHs)。到目前为止,多环芳烃是否会在南极高等鱼类的生理机能上留下印记,在很大程度上仍是未知的。我们通过两条途径来探讨这个问题:第一,我们研究了芳烃受体(Ahr)的功能反应,这是多环芳烃在生物群中产生许多毒性作用的分子起始事件。以南极高等鲈形目鱼类为代表,大西洋鳕鱼作为非极地参考物种。我们对鲈形目鱼类的芳烃受体配体结合域(LBD)进行了测序和克隆,并开展了基于GAL4的荧光素酶报告基因检测,以表达芳烃受体配体结合域。苯并[a]芘(BaP)、β-萘黄酮和屈被用作报告基因检测的配体。第二,我们研究了在急性、无细胞毒性的苯并[a]芘暴露期间,鲈形目鱼类分离肝细胞中芳烃受体激活的能量消耗。在报告基因检测中,大西洋鳕鱼和南极鲈形目鱼类的芳烃受体配体结合域被本文测试的配体激活。在对南极高等鲈形目鱼类分离肝细胞的体外检测中,苯并[a]芘暴露对整体呼吸没有影响,但导致了用于蛋白质合成的呼吸变化。因此,我们的研究表明,南极高等鱼类拥有功能性的芳烃受体,其可被环境污染物以浓度依赖的方式激活。这与细胞蛋白质合成成本的改变有关。未来的研究必须表明,芳烃受体途径的毒物诱导激活是否可能导致南极鱼类的机体性能改变。
在线版本包含可在10.1007/s00300-021-02992-4获取的补充材料。