Oxidative Stress-Induced DNA Damage by Manganese Dioxide Nanoparticles in Human Neuronal CellsReportar como inadecuado

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BioMed Research International - Volume 2017 2017, Article ID 5478790, 10 pages - https:-doi.org-10.1155-2017-5478790

Research ArticleDepartment of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia

Correspondence should be addressed to Daoud Ali

Received 20 December 2016; Revised 13 March 2017; Accepted 10 April 2017; Published 17 May 2017

Academic Editor: Davor Zeljezic

Copyright © 2017 Saud Alarifi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Metal nanoparticles have been extensively used in industry as well as in biomedical application. In this work, we have evaluated the toxic potential of manganese dioxide MnO2 nanoparticles MNPs on human neuronal SH-SY5Y cells. Cellular toxicity due to MNPs 0, 10, 30, and 60 μg-ml on the SH-SY5Y cell was observed by 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide MTT and neutral red uptake NRU tests. MNPs produced reactive oxygen species ROS and declined in mitochondrial membrane potential in the SH-SY5Y cell in dose and duration dependent manner. Moreover, lipid peroxide LPO, superoxide dismutase SOD, and catalase CAT activities were increased and glutathione was reduced in dose and time dependent manner. A significant upgrade in Hoechst 33342 fluorescence intensity chromosome condensation and phosphatidylserine translocation apoptotic cell was visualized in cells treated with MNPs for 48 h. On the other hand, caspase-3 activity was increased due to MNPs in SH-SY5Y cells. DNA strand breaks were determined by alkaline single cell gel electrophoresis assay Comet Assay and maximum fragmentation of DNA produced due to MNPs 60 μg-ml for 48 hours. This result provides a basic mechanism of induction of apoptosis and toxicity by MNPs in SH-SY5Y cells.

Autor: Saud Alarifi, Daoud Ali, and Saad Alkahtani

Fuente: https://www.hindawi.com/


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