Journal
TOXICOLOGY IN VITRO
Volume 24, Issue 1, Pages 45-55Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2009.09.007
Keywords
Nanoparticles; ZnO; Oxidative stress; Calcium modulation; Cytotoxicity; Gene expression
Categories
Funding
- Department of Biological Sciences
- cDNA Resource Center of the Missouri University of Science and Technology
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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 mu g/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. (C) 2009 Elsevier Ltd. All rights reserved.
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