RRC ID 67351
Author Fukui H, Iwahashi H, Nishio K, Hagihara Y, Yoshida Y, Horie M.
Title Ascorbic acid prevents zinc oxide nanoparticle-induced intracellular oxidative stress and inflammatory responses.
Journal Toxicol Ind Health
Abstract Exposure to zinc oxide nanoparticles (ZnO NPs) promotes acute pulmonary toxicity through oxidative stress and inflammation. Furthermore, dissolved zinc from ZnO NPs induces the formation of intracellular reactive oxygen species (ROS). We previously reported that supplemental ascorbic acid (AA) inhibits ZnO NP-induced acute pulmonary toxicity in a rat model; however, the mechanism of this action remains unclear. Therefore, we investigated the effects of AA on ZnO NP-induced cytotoxicity in human lung carcinoma A549 cells. AA was found to suppress intracellular production of ROS, and thus reduce the subsequent inflammation of ZnO NPs. However, intracellular Zn2+ concentrations were higher in AA-treated cells than in AA-untreated cells. AA was found to react with Zn2+ but not with the ZnO NPs themselves. These results suggest the possibility that AA-chelated extracellular Zn2+ and the Zn-AA complex was readily taken up into cell. Even if the intracellular Zn2+ level was high, cytotoxicity might be reduced because the Zn-AA complex was stable. Co-treatment of AA to A549 inhibited ROS production and subsequent intracellular inflammatory responses. These results are consistent with those previously reported from an in vivo model. Thus, two possibilities can be considered about the cytotoxicity-reducing the effect of AA: antioxidant efficacy and chelating effect.
Volume 33(9)
Pages 687-695
Published 2017-9-1
DOI 10.1177/0748233717707361
PMID 28854869
MeSH A549 Cells Antioxidants / pharmacology Ascorbic Acid / pharmacology* Humans Inflammation Metal Nanoparticles / toxicity* Oxidative Stress / drug effects Particle Size Reactive Oxygen Species / metabolism Zinc Oxide / toxicity*
Human and Animal Cells A549