Toxicity of carboxylated carbon nanotubes in endothelial cells is attenuated by stimulation of the autophagic flux with the release of nanomaterial in autophagic vesicles

Carboxylated multiwalled carbon nanotubes (CNTs) induce a decrease in viability of cultured human umbilical vein endothelial cells (HUVECs) associated with blockade of the autophagic flux with profound accumulation of autophagosomes visualized by the autophagosome marker LC3B-GFP. Stimulation of the autophagic flux with 1 nmol/L bafilomycin A1 (BafA1) attenuated the cytotoxicity of CNTs in HUVECs and was associated with the extracellular release of the nanomaterial in autophagic microvesicles.141