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Effects of waterborne Cu exposure in gilthead sea bream (Sparus aurata): a proteomic approach.

机译:金头鲷( Sparus aurata )中水性铜暴露的影响:一种蛋白质组学方法。

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摘要

Aquatic organisms may suffer from exposure to high Cu concentrations, since this metal is widely used in feed supplementation, in pesticide formulation and as antifouling. Chronic exposure to Cu, even at sub-lethal doses, may strongly affect fish physiology. To date, several biomarkers have been used to detect Cu exposure in fish producing contrasting results. Therefore, we used a proteomic approach to clarify how Cu exposure may affect the serum proteome of gilthead sea bream (Sparus aurata), since serum could be considered a good source of early-biomarkers of Cu toxicosis. For this purpose we exposed juvenile gilthead sea bream to waterborne Cu (0.5 mg/L). Our results indicate that fish tightly regulate circulating Cu levels, which are not affected by metal exposure. This homeostatic control is mainly achieved by the liver, able to excrete high amounts of the metal via bile. Cu exposure caused differential expression of several serum proteins, 10 of which were identified by Mascot and BLAST search. All these proteins, with the exception of growth hormone receptor and gamma -glutamyl-carboxylase, can be related to: (1) Cu-induced hepatotoxicity (cytochrome oxidase subunit I, alanine aminotransferase, glutathione S-transferase); (2) potential immunosuppression due to interference of Cu with the inflammation/immunity network ( alpha -1 antitrypsin, angiotensinogen, complement component C3, recombination-activating protein-1 and warm temperature acclimation-related 65 kDa protein).
机译:水生生物可能会暴露于高浓度的铜中,因为这种金属被广泛用于饲料补充,农药制剂和防污剂中。长期暴露于Cu,即使处于亚致死剂量也可能强烈影响鱼类的生理。迄今为止,已经使用了几种生物标记物来检测鱼中的铜暴露,从而产生相反的结果。因此,我们使用蛋白质组学方法阐明了铜暴露如何影响金头鲷( Sparus aurata )的血清蛋白质组,因为血清可以被认为是铜中毒的早期生物标志物的良好来源。为此,我们将少年金头鲷暴露于水性铜(0.5 mg / L)中。我们的结果表明,鱼类严格调节循环铜水平,不受金属暴露的影响。这种体内稳态控制主要是通过肝脏实现的,它能够通过胆汁排出大量的金属。铜暴露引起几种血清蛋白的差异表达,其中10种通过Mascot和BLAST搜索确定。除生长激素受体和γ-谷氨酰羧化酶外,所有这些蛋白都可能与以下方面有关:(1)铜诱导的肝毒性(细胞色素氧化酶亚基I,丙氨酸氨基转移酶,谷胱甘肽S-转移酶); (2)由于铜干扰炎症/免疫网络(α-1抗胰蛋白酶,血管紧张素原,补体成分C3,重组激活蛋白1和与温度适应有关的65 kDa蛋白)而引起的潜在免疫抑制作用。

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