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Histological assessment of systemic toxicity induced by zinc oxide nanoparticles and the prophylactic potency of ascorbate in albino rats
Amira Osman1, Said Mohamed Afify2, Amira Frag3, Sarah Mohammed Alghandour4
1 Department of Histology, Faculty of Medicine, Kafrelsheikh and Horus University, Kafrelsheikh, Egypt
2 Division of Biochemistry, Chemistry Department, Faculty of Science, Menoufia University, Al-Menoufia, Egypt
3 Department of Anatomy, Faculty of Medicine, Kafrelsheikh University, Kafrelsheikh, Egypt
4 Department of Histology, Faculty of Medicine, Cairo University, Cairo, Egypt
Correspondence Address:
Amira Osman,
Department of Histology, Faculty of Medicine, Kafrelsheikh and Horus University, Kafrelsheikh 33511
Egypt
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/jmau.jmau_68_22
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Background: Nanoparticles of zinc oxide (ZnO-NPs) are frequently implemented in cosmetics, additives, and electronic devices. Moreover, their applications extend to water treatment, drug delivery, and cancer therapy. As a result, NP toxicity became an essential subject in biosafety research. Aim: Using histological and immunohistochemical analysis, we attempted to investigate whether ascorbate (“vitamin C”) (VC) could protect liver, lung, and spleen tissues from ZnO-NP systemic toxicity. Materials and Methods: Rats were classified as control group, NP group injected intraperitoneally (IP), once by dissolved ZnO-NPs (200 mg/kg), and NP + VC group injected IP, once by dissolved ZnO-NPs (200 mg/kg) and then ingested 100 mg/kg of VC orally. Blood samples were collected. Liver, lung, and spleen specimens were prepared for light, electron microscopic, and immunohistochemical analysis. Results: In comparison to the control group, the NP group's liver enzyme, i.e. aspartate transaminase and alanine transaminase, values and counts of white blood cells (WBCs) were higher on the 7th day, but their red blood corpuscle (RBC) count, hemoglobin (Hgb) level, platelet count, and albumin values were lower. Histopathological analysis of liver, lung, and spleen tissues showed severe toxicity manifested by cell apoptosis, mononuclear cell infiltration, dilated blood vessels, and hemorrhage. In addition, the NP group showed a significantly higher expression of Ki67 and caspase-3 immunoreactivity. The biochemical, hematological, and histopathological results of the NP + VC group improved overall, reflecting VC's protective effect against systemic toxicity. Conclusion: Our study revealed that ascorbate (VC) inhibited the systemic toxicity prompted by ZnO-NPs in lung, liver, and spleen tissues, indicating its importance for future treatment with ZnO-NPs.
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