Intracellular degradation of functionalized carbon nanotube/iron oxide hybrids is modulated by iron via Nrf2 pathway.
Fiche publication
Date publication
janvier 2017
Journal
Scientific reports
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BEGIN-COLIN Sylvie, Dr MENARD-MOYON Cécilia, Dr BIANCO Alberto
Tous les auteurs :
Elgrabli D, Dachraoui W, Marmier H, Ménard-Moyon C, Bégin D, Bégin-Colin S, Bianco A, Alloyeau D, Gazeau F
Lien Pubmed
Résumé
The in vivo fate and biodegradability of carbon nanotubes is still a matter of debate despite tremendous applications. In this paper we describe a molecular pathway by which macrophages degrade functionalized multi-walled carbon nanotubes (CNTs) designed for biomedical applications and containing, or not, iron oxide nanoparticles in their inner cavity. Electron microscopy and Raman spectroscopy show that intracellularly-induced structural damages appear more rapidly for iron-free CNTs in comparison to iron-loaded ones, suggesting a role of iron in the degradation mechanism. By comparing the molecular responses of macrophages derived from THP1 monocytes to both types of CNTs, we highlight a molecular mechanism regulated by Nrf2/Bach1 signaling pathways to induce CNT degradation via NOX complex activation and O, HO and OH production. CNT exposure activates an oxidative stress-dependent production of iron via Nrf2 nuclear translocation, Ferritin H and Heme oxygenase 1 translation. Conversely, Bach1 was translocated to the nucleus of cells exposed to iron-loaded CNTs to recycle embedded iron. Our results provide new information on the role of oxidative stress, iron metabolism and Nrf2-mediated host defence for regulating CNT fate in macrophages.
Référence
Sci Rep. 2017 Jan 25;7:40997