Cerium and Yttrium Oxide Nanoparticles Against Lead-Induced Oxidative Stress and Apoptosis in Rat Hippocampus

Hosseini, A. and Sharifi, A.M. and Abdollahi, M. and Najafi, R. and Baeeri, M. and Rayegan, S. and Cheshmehnour, J. and Hassani, S. and Bayrami, Z. and Safa, M. (2015) Cerium and Yttrium Oxide Nanoparticles Against Lead-Induced Oxidative Stress and Apoptosis in Rat Hippocampus. Biological Trace Element Research, 164 (1). pp. 80-89.

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Due to numerous industrial applications, lead has caused widespread pollution in the environment; it seems that the central nervous system (CNS) is the main target for lead in the human body. Oxidative stress and programmed cell death in the CNS have been assumed as two mechanisms related to neurotoxicity of lead. Cerium oxide (CeO2) and yttrium oxide (Y2O3) nanoparticles have recently shown antioxidant effects, particularly when used together, through scavenging the amount of reactive oxygen species (ROS) required for cell apoptosis. We looked into the neuroprotective effects of the combinations of these nanoparticles against acute lead-induced neurotoxicity in rat hippocampus. We used five groups in this study: control, lead, CeO2 nanoparticles + lead, Y2O3 nanoparticles + lead, and CeO2 and Y2O3 nanoparticles + lead. Nanoparticles of CeO2 (1000 mg/kg) and Y2O3 (230 mg/kg) were administered intraperitoneally during 2 days prior to intraperitoneal injection of the lead (25 mg/kg for 3 days). At the end of the treatments, oxidative stress markers, antioxidant enzymes activity, and apoptosis indexes were investigated. The results demonstrated that pretreatments with CeO2 and/or Y2O3 nanoparticles recovered lead-caused oxidative stress markers (ROS, lipid peroxidation, and total thiol molecules) and apoptosis indexes (Bax/Bcl-2 and caspase-3 protein expression). Besides, these nanoparticles reduced the activities of lead-induced superoxide dismutase and catalase as well as the ADP/ATP ratio. Interestingly, the best recovery resulted from the compound of these nanoparticles. Based on these outcomes, it appears that this combination may potentially be beneficial for protection against lead-caused acute toxicity in the brain through improving the oxidative stress-mediated programmed cell death pathway. © 2014, Springer Science+Business Media New York.

Item Type: Article
Additional Information: cited By 21
Depositing User: eprints admin
Date Deposited: 01 Jul 2018 08:03
Last Modified: 01 Jul 2018 08:03
URI: http://eprints.iums.ac.ir/id/eprint/5373

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