Research Unit of Immuno-Microbiology Environmental and Carcinogenesis, Sciences Faculty of Bizerte, University of Carthage, Tunisia.
Research Unit of Immuno-Microbiology Environmental and Carcinogenesis, Sciences Faculty of Bizerte, University of Carthage, Tunisia.
Aquat Toxicol. 2018 Jul;200:21-27. doi: 10.1016/j.aquatox.2018.04.013. Epub 2018 Apr 23.
Oxidative stress is often implicated in nanoparticle toxicity. Several studies have highlighted the role of internalization routes in determining nanotoxicity. Here, we investigate how two endocytotic mechanisms (clathrin- and caveolae-mediated) impact on redox balance in gill and digestive gland of the mussel, Mytilus galloprovincialis. Animals were exposed (for 3, 6 and 12 h) to two sizes of silver nanoparticles (AgNP: <50 nm and <100 nm) prior to and after blockade of two endocytic pathways (amantadine blocks clathrin-mediated endocytosis while nystatin blocks caveolae-mediated endocytosis). Redox-proteomic tools were used to determine effects. Our results demonstrate the ability of both sizes of AgNP (<50 and <100 nm) to cause protein thiol oxidation and/or protein carbonylation. However, blockade of endocytotic routes mitigated AgNP toxicity. Differential ROS-related toxicity of AgNP to mussel tissues seemed to be linked to tissue-specific mode of action requirements. Cell uptake mechanism strongly influences toxicity of AgNPs in this filter-feeder.
氧化应激通常与纳米颗粒毒性有关。一些研究强调了内化途径在确定纳米毒性方面的作用。在这里，我们研究了两种内吞作用机制（网格蛋白和小窝介导）如何影响贻贝（贻贝）鳃和消化腺中的氧化还原平衡。在阻断两种内吞途径（金刚烷胺阻断网格蛋白介导的内吞作用，而制霉菌素阻断小窝介导的内吞作用）之前和之后，动物（暴露 3、6 和 12 小时）暴露于两种大小的银纳米颗粒（AgNP：<50nm 和<100nm）。使用氧化还原蛋白质组学工具来确定影响。我们的结果表明，两种大小的 AgNP（<50nm 和<100nm）都能够引起蛋白质巯基氧化和/或蛋白质羰基化。然而，内吞途径的阻断减轻了 AgNP 的毒性。AgNP 对贻贝组织的差异 ROS 相关毒性似乎与组织特异性作用模式要求有关。细胞摄取机制强烈影响这种滤食者中 AgNPs 的毒性。
