Titanium dioxide nanoparticles impair the inner blood-retinal barrier and retinal electrophysiology through rapid ADAM17 activation and claudin-5 degradation

Abstract Background Depending on their distinct properties, titanium dioxide nanoparticles (TiO 2 -NPs) are manufactured extensively and widely present in our daily necessities, with growing environmental release public concerns. In sunscreen formulations, supplementation of TiO -NPs may reach up to 25% (w/w). Ocular contact occur accidentally certain cases, allowing undesirable risks human vision. This study aimed understand the barrier integrity retinal endothelial cells response -NP exposure. bEnd.3 (HRECs) were exposed -NP, followed by examination tight junction components functions. Results TiO2-NP treatment apparently induced a broken structure junctional plaques, conferring decreased transendothelial electrical resistance, permeable paracellular cleft, improved cell migration vitro. might involve rapid activation metalloproteinase, disintegrin metalloproteinase 17 (ADAM17), ADAM17-mediated claudin-5 degradation. For vivo study, C57BL/6 mice administered single dose intravitreally then subjected complete ophthalmology examination. Fluorescein leakage reduced blood flow at optical disc indicated damaged inner blood-retinal -NPs. Inappreciable change thickness sublayers alleviated electroretinography amplitude observed -NP-treated eyes. Conclusions Overall, data demonstrate that can damage function, thereby affecting electrophysiology.