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Background Recently, silver nanoparticles (Ag-NPs) were shown to provoke oxidative stress through the release of reactive oxygen species and consequently induce cell damage. Selenium-loaded chitosan nanoparticles (CS-SeNPs) have anti-inflammatory and antioxidant effects, indicating that they ameliorate Ag-NPs-induced ovarian toxicity. Objective This study aimed to assess how well CS-SeNPs counteract the damaging effects of Ag-NPs on the ovarian tissue of adult female albino rats. Methods Forty mature female albino rats were divided into four equal groups: for 60 days, Group I (control) was given 0.5 ml/kg of distilled water; Group II was given Ag-NPs orally (100 mg/kg); Group III was given Ag-NPs orally (100 mg/kg/d) plus CS-SeNPs (0.5 mg/kg/d); and Group IV was given only CS-SeNPs orally (0.5 mg/kg/d). All the ovarian tissues were removed and underwent immunohistochemical, histological, and biochemical analyses. Results Ag-NPs-exposed rats revealed a marked reduction in reduced glutathione (GSH) and superoxide dismutase (SOD). Numerous histopathological alterations were found along with a significant increase in PCNA- and Caspase-3-immunoreactive cells. Most of these alterations were successfully ameliorated by CS-SeNPs, as indicated by marked increases in GSH and SOD. Conclusion CS-SeNPs ameliorate the toxic effects of Ag-NPs on the ovarian tissue of adult female albino rats.

Background: Mesenchymal stem cells (MSCs) have shown positive therapeutic effects on various diseases; however, their functionality can decline during in vitro expansion. Selenium (Se) supplementation has emerged as a strategy for enhancing MSC culture. This study evaluated the effects of different forms of selenium (Na2SeO4, SeMet, ebselen, and chitosan-coated selenium nanoparticles (CS-SeNPs)) on the biological functions of MSCs. Methods: Human umbilical cord-derived MSCs (HUC-MSCs) were cultured in media supplemented with various selenium compounds at specific concentrations. To investigate their biological effects, we assessed cell proliferation, morphology, surface marker expression, and differentiation potential. Furthermore, to elucidate the underlying mechanisms, we analyzed key markers of cellular senescence, including p16, p21, IL-6, IL-8, p27, p53, and reactive oxygen species (ROS) levels. Results: All the selenium treatments promoted hUC-MSC proliferation at specific concentrations. CS-SeNPs and Na2SeO4 exhibited relatively high bioavailability, whereas ebselen and SeMet demonstrated relatively low toxicity. The optimal concentration (0.5 μM CS-SeNPs or 0.25 μM Na2SeO4) significantly enhanced proliferation without altering the hUC-MSC morphology, phenotype, or differentiation capacity. Both CS-SeNPs and Na2SeO4 effectively promoted hUC-MSC proliferation and reduced the senescence of hUC-MSCs by downregulating key senescence-related effectors: the cell cycle inhibitors p16, p21, p27, and p53; and the levels of ROS and senescence-associated secretory phenotype factors (IL-6 and IL-8). Conclusions: Selenium supplementation is an effective strategy for improving MSC expansion and alleviating senescence. The beneficial effects are dependent on the specific selenium compound used, with CS-SeNPs and Na2SeO4 showing particularly strong potential for enhancing the bioavailability and function of hUC-MSCs during in vitro cultivation.