ArticleFrontiers in neuroscience2021
Ameliorative Role of Cerium Oxide Nanoparticles Against Fipronil Impact on Brain Function, Oxidative Stress, and Apoptotic Cascades in Albino Rats.
Article in Frontiers in neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 26 citations in OpenAlex.
- Potential effect of cerium oxide nanoparticles against boldenone-induced oxidative stress, inflammation, and reproductive dysfunction in male albino rats.Scientific reports · 2026Article
- Effects of quercetin-immobilized albumin cerium oxide nanoparticles on glutamate toxicity: in vitro study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Astaxanthin alleviates fipronil-induced neuronal damages in male rats through modulating oxidative stress, apoptosis, and inflammatory markers.Scientific reports · 2025Article
- Enhanced Cognitive and Behavioral Function as well as Neurobiochemical Enzyme Activities in Aluminum-Exposed Rats through Cerium Oxide Nanoparticles (CeOArchives of Razi Institute · 2025Article
- Influence of EuInternational journal of molecular sciences · 2024Article
- Neuroprotective effects of polyacrylic acid (PAA) conjugated cerium oxide against hydrogen peroxide- and 6-OHDA-induced SH-SY5Y cell damage.Scientific reports · 2023Article
- Infrared spectroscopy analysis determining secondary structure change in albumin by cerium oxide nanoparticles.Frontiers in toxicology · 2023Article
- Betanin ameliorates fipronil-induced nephrotoxicity via activation of Nrf2-HO-1/NQO-1 pathway in albino rat model.Toxicology research · 2022Article
- Activation of SIRT-1 Pathway by Nanoceria Sheds Light on Its Ameliorative Effect on Doxorubicin-Induced Cognitive Impairment (Chemobrain): Restraining Its Neuroinflammation, Synaptic Dysplasticity and Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Cerium oxide nanoparticles attenuate the renal injury induced by cadmium chloride via improvement of the NBN and Nrf2 gene expressions in rats.Toxicology research · 2022Article
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14 authors at 6 institutions in 4 countries.
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Abstract
Fipronil (FIP) is an N-phenylpyrazole insecticide that is used extensively in public health and agriculture against a wide range of pests. Exposure to FIP is linked to negative health outcomes in humans and animals including promoting neuronal cell injury, which results in apoptosis through the production of reactive oxygen species (ROS). Therefore, the purpose of the current study was to investigate the neuroprotective effects of cerium oxide nanoparticles (CeNPs) on neuronal dysfunction induced by FIP in albino rats. Male rats were randomly classified into four groups: control, FIP (5 mg/kg bwt), CeNPs (35 mg/kg bwt), and FIP + CeNPs (5 (FIP) + 35 (CeNPs) mg/kg bwt), which were treated orally once daily for 28 consecutive days. Brain antioxidant parameters, histopathology, and mRNA expression of genes related to brain function were evaluated. The results revealed oxidative damage to brain tissues in FIP-treated rats indicated by the elevated levels of malondialdehyde (MDA) and nitric oxide (NO) levels and reduced activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx). On the other hand, the FIP's group that was treated with CeNPs showed decrease in MDA and NO levels and increase in SOD and GPx enzymes activity. Besides, FIP-treated rats showed decreased butyrylcholinesterase (BuChE) activity in comparison to the FIP + CeNPs group. Moreover, FIP caused up-regulation of the expression of neuron-specific enolase (NSE), caspase-3, and glial fibrillary acidic protein (GFAP) but down-regulation of B-cell lymphoma-2 (BCL-2) expression. But the FIP + CeNPs group significantly down-regulated the GFAP, NSE, and caspase-3 and up-regulated the gene expression of BCL-2. Additionally, the FIP-treated group of rats had clear degenerative lesions in brain tissue that was reversed to nearly normal cerebral architecture by the FIP + CeNPs treatment. Immunohistochemical examination of brain tissues of rats-treated with FIP showed abundant ionized calcium-binding adaptor molecule 1 (Iba-1) microglia and caspase-3 and apoptotic cells with nearly negative calbindin and synaptophysin reaction, which were countered by FIP + CeNPs treatment that revealed a critical decrease in caspase-3, Iba-1 reaction with a strong calbindin positive reaction in most of the Purkinje cells and strong synaptophysin reaction in the cerebrum and cerebellum tissues. Based on reported results herein, CeNPs treatment might counteract the neurotoxic effect of FIP pesticide via an antioxidant-mediated mechanism.
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