The ameliorative effect of nanoselenium on histopathological and biochemical alterations induced by melamine toxicity on the brain of adult male albino rats

•Melamine causes neurodegeneration in brain parts; cerebrum, hippocampus and cerebellum.•The neurotoxicity mechanism of melamine is through induction of oxidative stress and apoptosis.•Biochemically, melamine administration significantly decreased the total antioxidant capacity (TAC) in serum.•Also,...

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Veröffentlicht in:Neurotoxicology (Park Forest South) 2021-09, Vol.86, p.37-51
Hauptverfasser: Bashir, Dina W., Rashad, Maha M., Ahmed, Yasmine H., Drweesh, Elsayed A., Elzahany, Eman A.M., Abou-El-Sherbini, Khaled S., EL‐Leithy, Ebtihal M.M.
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Sprache:eng
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Zusammenfassung:•Melamine causes neurodegeneration in brain parts; cerebrum, hippocampus and cerebellum.•The neurotoxicity mechanism of melamine is through induction of oxidative stress and apoptosis.•Biochemically, melamine administration significantly decreased the total antioxidant capacity (TAC) in serum.•Also, melamine significantly induced down-regulation of Nrf2 and GPX expression.•Selenium nanoparticles has a protective role against melamine induced neurotoxicity. Melamine is a chemical substance used as a food adulterant because of its high nitrogen content; it is known to induce neurotoxicity, thereby adversely affecting the central nervous system. The biocompatibility, bioavailability, lower toxicity, and the large surface area of nanosized selenium relative to its other forms indicate that selenium nanoparticles (SeNPs) have a potential ameliorative effect against melamine-induced neurotoxicity. In this study, we tested this hypothesis using 40 adult male albino rats that were randomly assigned into four groups (n = 10 per group): group I rats served as the untreated negative controls and were fed with standard diet and distilled water; group II rats were orally treated with melamine (300 mg/kg body weight/d); group III rats orally received melamine (300 mg/kg body weight/d) and SeNPs (2 mg/kg body weight/d); and group IV rats received SeNPs only (2 mg/kg body weight/d) for 28 days. Blood and brain samples were collected from all rats and processed for biochemical, histopathological, and immunohistochemical investigations. SeNPs were encapsulated in starch as a natural stabilizer and a size-controlling agent (SeNP@starch). The prepared SeNPs were characterized using different techniques. Inductively coupled plasma-optical emission spectrometry (ICP-OES) indicated that the percentage of selenium loaded in starch was 1.888 %. Powder x-ray diffractometer (XRD) was used to investigate the crystalline structure of the Se-NP@starch, to be tubular and composed of amorphous starch as well as metallic selenium. Thermogravimetric analysis confirmed the thermal stability of the product and determined the interactions among the different components. Transmission electron microscope demonstrated the spherical shape of SeNPs and their dispersion into starch surface as well as evaluating their size in nanoscale (range 20−140 nm). Our results revealed that the melamine- exposed rats had significantly elevated in malondialdehyde levels, significantly reduced in total antioxida
ISSN:0161-813X
1872-9711
DOI:10.1016/j.neuro.2021.06.006