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Toxics 2018, 6(2), 29; https://doi.org/10.3390/toxics6020029

Zinc Oxide Nanoparticles Induced Oxidative DNA Damage, Inflammation and Apoptosis in Rat’s Brain after Oral Exposure

1
Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11495, Saudi Arabia
2
Department of Biochemistry, Faculty of Pharmacy, Mansoura University, Mansoura 35516, Egypt
3
Department of Medical Biochemistry, Faculty of Medicine, Alexandria University, Alexandria 21111, Egypt
4
Department of Medical Biotechnology, Institute of Genetic Engineering City of Scientific Research and biotechnological applications, Borg El Arab, Alexandria 21111, Egypt
*
Author to whom correspondence should be addressed.
Received: 23 April 2018 / Revised: 11 May 2018 / Accepted: 19 May 2018 / Published: 26 May 2018
(This article belongs to the Special Issue Nanoparticles Toxicity and Impacts on Biodiversity)
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Abstract

Growing evidences demonstrated that zinc oxide nanoparticles (ZnONPs) could reach the brain after oral ingestion; however, the “neurotoxicity of” ZnONPs after oral exposure has not been fully investigated. This study aimed to explore the “neurotoxicity of” ZnONPs (<100 nm) after oral exposure to two doses; 40 and 100 mg/kg for 24 h and 7 days. The exposure to 40 and 100 mg/kg of ZnONPs for 24 h did not elicit “neurotoxicity” compared to normal control. However, the daily exposure to both doses for 7 days caused oxidative stress in brain tissue as detected by the elevation of the levels of malondialdehyde, the main product of lipid peroxidation and nitrite as an index of nitric oxide with concomitant decline in the concentrations of antioxidants. In addition, both doses resulted in DNA fragmentation which was confirmed by increased percentage of tailed DNA, DNA tail intensity and length and tail moment particularly with the dose 100 mg/kg. Moreover, both doses led to the elevation of the inflammatory cytokines along with increased apoptotic markers including caspase-3 and Fas. Heat shock protein-70 levels were also elevated possibly as a compensatory mechanism to counteract the ZnONPs-induced oxidative stress and apoptosis. The present results indicate the “neurotoxicity of” ZnONPs after recurrent oral exposure via oxidative stress, genotoxicity, inflammatory response and apoptosis. View Full-Text
Keywords: ZnONPs; brain; DNA fragmentation; oxidative stress; heat shock protein-70; interleukin-1β; caspase-3; Fas ZnONPs; brain; DNA fragmentation; oxidative stress; heat shock protein-70; interleukin-1β; caspase-3; Fas
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Attia, H.; Nounou, H.; Shalaby, M. Zinc Oxide Nanoparticles Induced Oxidative DNA Damage, Inflammation and Apoptosis in Rat’s Brain after Oral Exposure. Toxics 2018, 6, 29.

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