ArticleOxidative medicine and cellular longevity2020
Selenium Protects against Zearalenone-Induced Oxidative Stress and Apoptosis in the Mouse Kidney by Inhibiting Endoplasmic Reticulum Stress.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 49 citations in OpenAlex.
- Toxicity analysis of food contaminants based on network toxicology and molecular docking: A case study of Zearalenone.PloS one · 2026Article
- The protective role of selenium against high-fructose corn syrup-induced kidney damage: a histopathological and molecular analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Review
- Ferroptosis and its emerging role in kidney stone formation.Molecular biology reports · 2024Review
- Effect of mesenchymal stem cells and polyvinyl alcohol-coated selenium nanoparticles on rats with Alzheimer-like phenotypes.Iranian journal of basic medical sciences · 2024Article
- Dietary Coated Sodium Butyrate Ameliorates Hepatic Lipid Accumulation and Inflammation via Enhancing Antioxidative Function in Post-Peaking Laying Hens.Metabolites · 2023Article
- CRISPR-activation screen identified potassium channels for protection against mycotoxins through cell cycle progression and mitochondrial function.Cell stress · 2023Article
- Article
- Dietary Selenium Intake and Kidney Stones in Old Adults: an Analysis from NHANES 2011 to 2018.Biological trace element research · 2023Article
- Crosstalk between Mycotoxins and Intestinal Microbiota and the Alleviation Approach via Microorganisms.Toxins · 2022Review
- Sodium selenite attenuates zearalenone-induced apoptosis through inhibition of endoplasmic reticulum stress in goat trophoblast cells.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2022Article
- Review
- Selenium Attenuates TBHP-Induced Apoptosis of Nucleus Pulposus Cells by Suppressing Mitochondrial Fission through Activating Nuclear Factor Erythroid 2-Related Factor 2.Oxidative medicine and cellular longevity · 2022Article
- Current Strategies and Potential Prospects for Nanoparticle-Mediated Treatment of Diabetic Nephropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Review
- Selenium-chitosan alleviates the toxic effects of Zearalenone on antioxidant and immune function in mice.Frontiers in veterinary science · 2022Article
- Protective and detoxifying effects conferred by selenium against mycotoxins and livestock viruses: A review.Frontiers in veterinary science · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study assessed the molecular mechanism of selenium (Se) protecting against kidney injury induced by zearalenone (ZEA) in mice. The experimental mice were divided into 4 groups including the control group, the Se group, the ZEA group, and the Se+ZEA group; ZEA and Se were administered orally for 28 days. The changes in renal biochemical index (BUN, UA, and CRE), biochemical change of kidney damage such as BUN, UA, and CRE, and oxidative damage such as MDA, T-SOD, and GSH-Px were investigated. Pathological sections and TUNEL staining were used to analyze renal pathological changes and cell apoptosis. qRT-PCR and Western blot were employed to detect the expression of genes and proteins which were related with endoplasmic reticulum stress. The results showed that ZEA increased the concentration of BUN, UA, and CRE and the content of MDA and decreased the activities of T-SOD and GSH-Px in the mouse kidneys. However, Se reversed above changes of the biochemical and antioxidant indexes of renal injury. Moreover, the results also showed that ZEA can increase the expression of Bax, caspase-12, caspase-3, Bip, CHOP, JNK protein, and mRNA and decrease the expression of Bcl-2 protein and mRNA. But Se reversed these proteins and genes related to endoplasmic reticulum stress and apoptosis. It can be concluded that Se protected against the kidney damage induced by ZEA. Se may protect the kidney from ZEA-induced apoptosis and oxidative stress by inhibiting ERS.
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