Fiche publication
Date publication
octobre 2015
Journal
ACS nano
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BEGIN-COLIN Sylvie
,
Dr MENARD-MOYON Cécilia
,
Dr BIANCO Alberto
Tous les auteurs :
Elgrabli D, Dachraoui W, Ménard-Moyon C, Liu XJ, Bégin D, Bégin-Colin S, Bianco A, Gazeau F, Alloyeau D
Lien Pubmed
Résumé
Despite numerous applications, the cellular-clearance mechanism of multiwalled carbon nanotubes (MWCNTs) has not been clearly established yet. Previous in vitro studies showed the ability of oxidative enzymes to induce nanotube degradation. Interestingly, these enzymes have the common capacity to produce reactive oxygen species (ROS). Here, we combined material and life science approaches for revealing an intracellular way taken by macrophages to degrade carbon nanotubes. We report the in situ monitoring of ROS-mediated MWCNT degradation by liquid-cell transmission electron microscopy. Two degradation mechanisms induced by hydroxyl radicals were extracted from these unseen dynamic nanoscale investigations: a non-site-specific thinning process of the walls and a site-specific transversal drilling process on pre-existing defects of nanotubes. Remarkably, similar ROS-induced structural injuries were observed on MWCNTs after aging into macrophages from 1 to 7 days. Beside unraveling oxidative transformations of MWCNT structure, we elucidated an important, albeit not exclusive, biological pathway for MWCNT degradation in macrophages, involving NOX2 complex activation, superoxide production, and hydroxyl radical attack, which highlights the critical role of oxidative stress in cellular processing of MWCNTs.
Mots clés
Animals, Cell Line, Humans, Macrophages, drug effects, Male, Membrane Glycoproteins, metabolism, NADPH Oxidase 2, NADPH Oxidases, metabolism, Nanotubes, Carbon, analysis, Oxidative Stress, drug effects, Rats, Sprague-Dawley, Reactive Oxygen Species, metabolism
Référence
ACS Nano. 2015 Oct 27;9(10):10113-24
