Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2603525 | Toxicology in Vitro | 2010 | 11 Pages |
The influence of 20 nm ZnO nanoparticles on cytotoxicity, oxidative stress, intracellular calcium homeostasis, and gene expression was studied in human bronchial epithelial cells (BEAS-2B). ZnO caused a concentration- and time-dependent cytotoxicity while elevating oxidative stress and causing membrane damage (cellular LDH release). There was a remarkably steep relationship between concentration and toxicity at concentrations from 5 to 10 μg/ml. Cytotoxicity was completely abolished by the antioxidant N-acetylcysteine (NAC). Exposure to ZnO also increased intracellular calcium levels ([Ca2+]in) in a concentration- and time-dependent manner that was partially attenuated by NAC. Nifedipine, a calcium channel blocker, partially attenuated the elevated [Ca2+]in, indicating that some of the excess [Ca2+]in is a result of influx from outside the cell. The relationships between oxidative stress, [Ca2+]in, and cytotoxicity are discussed. Exposure to a sublethal concentration of ZnO increased the expression of four genes that are involved in apoptosis and oxidative stress responses BNIP, PRDX3, PRNP, and TXRND1, by at least 2.5-fold. Thus, ZnO alters transcriptional regulation in BEAS-2B cells.