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Title of Journal: J Nanopart Res

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Abbravation: Journal of Nanoparticle Research

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Springer Netherlands

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DOI

10.1016/0016-5085(92)90857-u

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1572-896X

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TiOSubscript2/Subscript nanoparticleinduced R

Authors: Melissa A MaurerJones Jenna R Christenson Christy L Haynes
Publish Date: 2012/11/18
Volume: 14, Issue: 12, Pages: 1291-
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Abstract

Design of nontoxic nanoparticles will be greatly facilitated by understanding the nanoparticlecell interaction mechanism on a cell function level Mast cells are important cells for the immune system’s first line of defense and we can utilize their exocytotic behavior as a model cellular function as it is a conserved process across cell types and species Perturbations in exocytosis can also have implications for whole organism health One proposed mode of toxicity is nanoparticleinduced reactive oxygen species ROS particularly for titanium dioxide TiO2 nanoparticles Herein we have correlated changes in ROS with the perturbation of the critical cell function of exocytosis using UV light to induce greater levels of ROS in TiO2 exposed cells The primary culture mouse peritoneal mast cells MPMCs were exposed to varying concentrations of TiO2 nanoparticles for 24 h ROS content was determined using 27dihydrodichlorofluorescein diacetate DCFDA Cellular viability was determined with the MTT and Trypan blue assays and exocytosis was measured by the analytical electrochemistry technique of carbonfiber microelectrode amperometry MPMCs exposed to TiO2 nanoparticles experienced a dosedependent increase in total ROS content While there was minimal impact of ROS on cellular viability there is a correlation between ROS amount and exocytosis perturbation As nanoparticleinduced ROS increases there is a significant decrease 45  in the number of serotonin molecules being released during exocytosis increase 26  in the amount of time for each exocytotic granule to release and decrease 28  in the efficiency of granule trafficking and docking This is the first evidence that nanoparticleinduced ROS correlates with chemical messenger molecule secretion possibly making a critical connection between functional impairment and mechanisms contributing to that impairmentWe acknowledge Sarah Connolly a summer research undergraduate at the University of Minnesota for her work on developing ROS assay protocols and Diana Freeman for her help in isolating the MPMCs This research was financially supported by a grant from the National Science Foundation CHE0645041 and a National Science Foundation Graduate Research Fellowship awarded to MAMJ

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