Role of endocytotic uptake routes in impacting the ROS-related toxicity of silver nanoparticles to Mytilus galloprovincialis: a redox proteomic investigation
Role of endocytotic uptake routes in impacting the ROS-related toxicity of silver nanoparticles to Mytilus galloprovincialis: a redox proteomic investigation
Bouallegui, Younes; Ben Younes, Ridha; Oueslati, Ridha; Sheehan, David
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Restriction lift date:2020-04-23
Citation:Bouallegui, Y., Ben Younes, R., Oueslati, R. and Sheehan, D. (2018) 'Role of endocytotic uptake routes in impacting the ROS-related toxicity of silver nanoparticles to Mytilus galloprovincialis: a redox proteomic investigation', Aquatic Toxicology. doi: 10.1016/j.aquatox.2018.04.013
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.
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