Laboratory of Radioecology and Ecotoxicology, Institute of Radioprotection and Nuclear Safety, Bd 186, BP 3, 13115 Saint-Paul-Lez-Durance, France.
Ecotoxicol Environ Saf. 2012 Apr;78:218-24. doi: 10.1016/j.ecoenv.2011.11.026. Epub 2011 Dec 7.
We examined the impacts of Uranium (U) on mitochondria and on the response of antioxidants in the gills and the hepatopancreas of crayfish Procambarus clarkii after long-term exposure (30 and 60 days) to an environmentally relevant concentration (30 μg U/L). The expression of mitochondrial genes (12s, atp6, and cox1), as well as the genes involved in oxidative stress responses (sod(Mn) and mt) were evaluated. The activities of antioxidant enzymes (SOD, CAT, GPX and GST) were also studied. U accumulation in organs induced changes in genes' expression. The evolution of these transcriptional responses and differences between gene expression levels at high and low doses of exposure were also discussed. This study demonstrated that, after long-term exposure, U caused a decrease in antioxidant activities and induced oxidative stress. A possible ROS-mediated U cytotoxic mechanism is proposed. Expression levels of the investigated genes can possibly be used as a tool to evaluate U toxicity and seem to be more sensitive than the enzymatic activities. However a multiple biomarker approach is recommended as the perturbed pathways and the mode of action of this pollutant are not completely understood.
我们研究了铀(U)对螯虾(Procambarus clarkii)鳃和肝胰腺线粒体的影响,以及长期暴露(30 和 60 天)于环境相关浓度(30μg U/L)下抗氧化剂反应。评估了线粒体基因(12s、atp6 和 cox1)以及参与氧化应激反应的基因(sod(Mn)和 mt)的表达。还研究了抗氧化酶(SOD、CAT、GPX 和 GST)的活性。器官中 U 的积累引起了基因表达的变化。还讨论了这些转录反应的演变以及高剂量和低剂量暴露之间基因表达水平的差异。本研究表明,长期暴露后,U 会降低抗氧化活性并诱导氧化应激。提出了一种可能的 ROS 介导的 U 细胞毒性机制。研究的基因表达水平可能可用作评估 U 毒性的工具,并且似乎比酶活性更敏感。然而,建议采用多生物标志物方法,因为这种污染物的干扰途径和作用模式尚未完全了解。