Endocytosis, oxidative stress and IL-8 expression in human lung epithelial cells upon treatment with fine and ultrafine TiO2: role of the specific surface area and of surface methylation of the particles.

摘要: Inhaled ultrafine particles show considerably stronger pulmonary inflammatory effects when tested at equal mass dose with their fine counterparts. However, the responsible mechanisms are not yet fully understood. We investigated role of particle size and surface chemistry in initiating pro-inflammatory vitro A549 human lung epithelial cells on treatment different model TiO(2) particles. Two samples TiO(2), i.e. (40-300 nm) (20-80 were native forms as well upon methylation, was confirmed by Fourier transformed infrared spectroscopy. Radical generation during cell determined electron paramagnetic resonance 5,5-dimethyl-1-pyrroline-N-oxide or 4-hydroxy-2,2,6,6-tetramethylpiperidine-1-oxyl. Interleukin-8 mRNA expression/release RT-PCR ELISA, whereas uptake evaluated transmission microscopy. rapidly taken up cells, generally membrane bound aggregates large intracellular vesicles, vacuoles lamellar bodies. Aggregate tended to be smaller for also methylated compared non-methylated TiO(2). No observed inside nuclei any other vital organelle. Both but counterparts elicited significantly oxidant IL-8 release, despite aggregation state irrespective methylation. The present data indicate that even aggregates/agglomerates, can trigger responses appear driven area. Furthermore, our results these result from oxidants generated particle-cell interactions through a elucidated mechanism(s).