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Chromium oxide nanoparticle‐induced genotoxicity and p53‐dependent apoptosis in human lung alveolar cells
Author(s) -
Senapati Violet Aileen,
Jain Abhishek Kumar,
Gupta Govind Sharan,
Pandey Alok Kumar,
Dhawan Alok
Publication year - 2015
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.3174
Subject(s) - genotoxicity , apoptosis , micronucleus test , dna damage , reactive oxygen species , comet assay , chemistry , nanotoxicology , micronucleus , a549 cell , microbiology and biotechnology , toxicity , biophysics , biochemistry , biology , dna , organic chemistry
Chromium oxide (Cr 2 O 3 ) nanoparticles (NPs) are being increasingly used as a catalyst for aromatic compound manufacture, abrading agents and as pigments (e.g., Viridian). Owing to increased applications, it is important to study the biological effects of Cr 2 O 3 NPs on human health. The lung is one of the main exposure routes to nanomaterials; therefore, the present study was designed to determine the genotoxic and apoptotic effect of Cr 2 O 3 NPs in human lung epithelial cells (A549). The study also elucidated the molecular mechanism of its toxicity. Cr 2 O 3 NPs led to DNA damage, which was deduced by comet assay and cytokinesis block micronucleus assay. The damage could be mediated by the increased levels of reactive oxygen species. Further, the oxygen species led to a decrease in mitochondrial membrane potential and an increase in the ratio of BAX/Bcl‐2 leading to mitochondria‐mediated apoptosis induced by Cr 2 O 3 NPs, which ultimately leads to cell death. Hence, there is a need of regulations to be imposed in NP usage. The study provided insight into the caspase‐dependent mechanistic pathway of apoptosis. Copyright © 2015 John Wiley & Sons, Ltd.