Selenium Protects Retinal Cells from Cisplatin-Induced Alterations in Carbohydrate Residues
Selenium Protects Retinal Cells from Cisplatin-Induced Alterations in Carbohydrate Residues
Background: Investigate alterations in the expression and localization of carbohydrate units in rat retinal cells exposed to cisplatin toxicity. Aims: The aim of the study was to evaluate putative protec-tive effects of selenium on retinal cells subjected to cisplatin. Study Design: Animal experiment.Methods:EighteenhealthyWistarratsweredividedinto three equal groups: 1. Control, 2. Cisplatin and 3. Cisplatin+selenium groups. After anesthesia, the right eye of each rat was enucleated. Results: Histochemically, retinal cells of control groups reacted with ?-2,3-bound sialic acid-specific Maackia amu-rensis lectin (MAA) strongly, while cisplatin reduced the staining intensity for MAA. However, selenium administra-tion alleviated the reducing effect of cisplatin on the bind-ing sites for MAA in retinal cells. The staining intensity for N-acetylgalactosamine (GalNAc residues) specific Griffo-nia simplicifolia-1 (GSL-1) was relatively slight in control animals and cisplatin reduced this slight staining for GSL-1 further. Selenium administration mitigated the reducing ef-fect of cisplatin on the binding sites for GSL-1. A diffuse staining for N-acetylglucosamine (GlcNAc) specific wheat germ agglutinin (WGA) was observed throughout the retina of the control animals. In particular, cells localized in the in-ner plexiform and photoreceptor layers are reacted strongly with WGA. Compared to the control animals, binding sites for WGA in the retina of rats given cisplatin were remark-ably decreased. However, the retinal cells of rats given sele-nium reacted strongly with WGA. Conclusion: Cisplatin reduces ?-2,3-bound sialic acid, GlcNAc and GalNAc residues in certain retinal cells. How-ever, selenium alleviates the reducing effect of cisplatin on carbohydrate residues in retinal cells
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