Early stress responses in Atlantic salmon (Salmo salar) exposed to environmentally relevant concentrations of uranium

详细信息	查看全文 | 推荐本文 |

• 作者：You Song^a ; ^{you.song@umb.no} ; Brit Salbu^a ; Lene Sø ; rlie Heier^a ; Hans-Christian Teien^a ; Ole-Christian Lind^a ; Deborah Oughton^a ; Karina Petersen^b ; Bjø ; rn Olav Rosseland^c ; Lindis Skipperud^a ; Knut Erik Tollefsen^a ; ^b
• 关键词：Uranium ; Atlantic salmon ; Gene expression ; Micronuclei ; Biomarker ; Toxicological pathway
• 刊名：Aquatic Toxicology
• 出版年：2012
• 期刊代码：19_0166445x
• 类别：abs
• 出版时间：15 May, 2012
• 卷：112-113
• 期：Complete
• 页码：62-71
• 文件大小：721 K

摘要

Uranium (U) is a naturally occurring heavy metal widely used in many military and civil applications. Uranium contamination and the associated potential adverse effects of U on the aquatic environment have been debated during recent years. In order to understand the effect and mode of action (MoA) of U in vivo, juvenile Atlantic salmon (Salmo salar) were exposed to 0.25 mg/L, 0.5 mg/L and 1.0 mg/L waterborne depleted uranyl acetate, respectively, in a static system for 48 h. The U concentrations in the gill and liver were analyzed by inductively coupled plasma mass spectrometry (ICP-MS) and the resulting biological effects were determined by a combination of analysis of gene expression and micronuclei formation. The hepatic transcriptional level of 12 biomarker genes from four stress-response categories, including oxidative stress (纬-glutamyl cysteine synthetase (GCS), glutathione reductase (GR), glutathione peroxidase (GPx)), DNA damage and repair (P53, cyclin-dependent kinase inhibitor 1 (P21), growth arrest and DNA damage-inducible gene gamma (Gadd45G), proliferating cell nuclear antigen (PCNA), Rad51), apoptosis (Bcl2-associated X protein (BAX), Bcl-x, Caspase 6A,) and protein degradation (Ubiquitin) were evaluated by quantitative real-time polymerase chain reaction (q-rtPCR). The results clearly showed accumulation of U in the gill and liver with increasing concentrations of U in the exposure water. The effects of U on differential hepatic gene expression also occurred in a concentration-dependent manner, although deviations from ideal concentration-response relationships were observed at the highest U concentration (1.0 mg/L). All the genes tested were found to be up-regulated by U while no significant micronuclei formation was identified. The results suggest that U may cause oxidative stress in fish liver at concentrations greater than 0.25 mg/L, giving rise to clear induction of several toxicologically relevant biomarker genes, although no significant adverse effects were observed after the relatively short exposure period.