ArticleMolecular biology reports2019
Sodium selenite protects from 3-nitropropionic acid-induced oxidative stress in cultured primary cortical neurons.
Article in Molecular biology reports, 2019. 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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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Opposite Effects of Small and Large Diameter Selenium Nanoparticles on the Redox-Status and Survival of Cortical Cells in Toxic Models In Vitro.Biological trace element research · 2026Article
- Neuroprotective effects of silymarin in 3-nitropropionic acid-induced neurotoxicity in male mice: improving behavioral deficits by attenuating oxidative stress and neuroinflammation.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Comparison of mouse ovarian follicular development and gene expression in the presence of ovarian tissue extract and sodium selenite: An experimental study.International journal of reproductive biomedicine · 2023Article
- Effect of methylmercury on fetal neurobehavioral development: an overview of the possible mechanisms of toxicity and the neuroprotective effect of phytochemicals.Archives of toxicology · 2022Review
- Review
- Decrease in ovarian reserve through the inhibition of SIRT1-mediated oxidative phosphorylation.Aging · 2022Article
- Identification of cyclin D1 as a major modulator of 3-nitropropionic acid-induced striatal neurodegeneration.Neurobiology of disease · 2022Article
- Ovarian Oxidative Stress Induced Follicle Depletion After Zona Pellucida 3 Vaccination Is Associated With Subfertility in BALB/c Mice.Frontiers in veterinary science · 2022Article
- Potential Effects of Melatonin and Micronutrients on Mitochondrial Dysfunction during a Cytokine Storm Typical of Oxidative/Inflammatory Diseases.Diseases (Basel, Switzerland) · 2021Review
- The Effect of Sodium Selenite on Expression of Mitochondrial Transcription Factor A duringAvicenna journal of medical biotechnologyArticle
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Selenium (Se) is an essential trace element for humans; its intake is needed to allow the proper synthesis of 25 different selenoproteins that are necessary to the normal functioning of several organs, including the brain. Accordingly, decreased Se levels have been associated with neurological disorders. In the present study, we investigated the potential beneficial effects of Se, as sodium selenite, against 3-nitropropionic acid (3-NP)-induced oxidative stress in primary cultures of mouse cortical neurons. 3-NP treatment caused a significant decrease in cellular viability, which was accompanied by decreases in mitochondrial complex II activity and reduced glutathione (GSH) content, as well as increases in reactive oxygen species (ROS) generation and oxidized glutathione (GSSG) levels. Sodium selenite pretreatment (6 days) attenuated 3-NP-induced decrease in cell viability. In addition, sodium selenite pretreatment significantly protected against 3-NP-induced increase in ROS generation and decrease in GSH/GSSG ratio. Of note, sodium selenite pretreatment did not change 3-NP-induced decrease of mitochondrial complex II activity, suggesting that Se modulates secondary events resultant from 3-NP-induced mitochondrial dyshomeostasis. In addition, sodium selenite pretreatment significantly increased glutathione peroxidase (GPx) activity. Our data provide insights into the mechanism of protection by sodium selenite, which is related, at least in part, to GPx induction.
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