Nanosized Zinc Oxide Induces Toxicity in Human Lung Cells
Author(s) -
Devashri Sahu,
G. M. Kannan,
R. Vijayaraghavan,
T. Anand,
Farhath Khanum
Publication year - 2013
Publication title -
isrn toxicology
Language(s) - English
Resource type - Journals
eISSN - 2090-6196
pISSN - 2090-6188
DOI - 10.1155/2013/316075
Subject(s) - oxidative stress , toxicity , viability assay , apoptosis , metallothionein , dna fragmentation , programmed cell death , dna damage , chemistry , zinc , cell , fragmentation (computing) , nanotoxicology , microbiology and biotechnology , biophysics , biochemistry , biology , dna , ecology , organic chemistry
Zinc oxide nanoparticles (ZnO-NPs) are increasingly used in sunscreens, biosensors, food additives, pigments, rubber manufacture, and electronic materials. With the wide application of ZnO-NPs, concern has been raised about its unintentional health and environmental impacts. This study investigates the toxic effects of ZnO-NPs in human lung cells. In order to assess toxicity, human lung epithelial cells (L-132) were exposed to dispersion of 50 nm ZnO-NPs at concentrations of 5, 25, 50, and 100 μ g/mL for 24 h. The toxicity was evaluated by observing changes in cell morphology, cell viability, oxidative stress parameters, DNA damage analysis, and gene expression. Exposure to 50 nm ZnO-NPs at concentrations between 5 and 100 μ g/mL decreased cell viability in a concentration-dependent manner. Morphological examination revealed cell shrinkage, nuclear condensation, and formation of apoptotic bodies. The oxidative stress parameters revealed significant depletion of GSH level and increase in ROS levels suggesting generation of oxidative stress. ZnO-NPs exposure caused DNA fragmentation demonstrating apoptotic type of cell death. ZnO-NPs increased the expression of metallothionein gene, which is considered as a biomarker in metal-induced toxicity. To summarize, ZnO-NPs cause toxicity in human lung cells possibly through oxidative stress-induced apoptosis.
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