| Literature DB >> 30284226 |
Akram Ranjbar1, Sara Soleimani Asl2, Farzin Firozian3, Hamid Heidary Dartoti4, Saman Seyedabadi5, Masoumeh Taheri Azandariani1, Maziar Ganji6,7.
Abstract
Paraquat (PQ), as a widely used herbicide, enhances the formation of free radicals and oxidative stress. Cerium oxide nanoparticles (CeNPs) are one of the most utilized and effective nanoparticles having strong antioxidative properties and inhibiting free radicals. Here, we aimed to investigate the effects of CeNPs on brain oxidative toxic stress injury induced with PQ. The male rats were treated intraperitoneally daily with PQ (50 mg/kg/day) and CeNPs (15, 30, and 60 mg/kg/day) alone or in combination for 2 weeks. After treatments, the brain tissue samples were collected. Oxidative toxic stress biomarkers including lipid peroxidation (LPO), total antioxidant capacity (TAC), and total thiol molecules (TTM) as well as DNA damage and caspase-3 levels were measured. Moreover, the mRNA expression levels of Nestin and Neurod1 were assayed. Our results showed that PQ has significantly increased brain LPO, DNA damage, and caspase-3 levels and further reduced TAC and TTM contents, as well as expression levels of Nestin and Neurod1, compared with the control group (injection of saline). CeNPs (15- and 30-mg/kg doses) in groups co-administered with PQ significantly ameliorated the LPO, DNA damage, and caspase-3 levels while increasing TAC and TTM contents as well as enhancing Nestin and Neurod1 mRNA expression levels in the brain samples (P < 0.05). These findings suggest a neuroprotective and antioxidant role for CeNPs in PQ-induced brain injury. However, further studies are required to clarify its clinical/pharmacological significance.Entities:
Keywords: Apoptosis; Brain; Cerium oxide nanoparticle; DNA damage; Oxidative stress; Paraquat
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Year: 2018 PMID: 30284226 DOI: 10.1007/s12031-018-1191-2
Source DB: PubMed Journal: J Mol Neurosci ISSN: 0895-8696 Impact factor: 3.444