BACKGROUND AND AIMS: It has been hypothesized that Se depletion followed by decreased activity of Se-dependent enzymes may be responsible for the development of oxidative stress observed in various neurodegenerative diseases. Thus, Se-dependent protection strategy to reduce neuronal oxidative injuries, can contribute to attenuation of neurodegeneration. The compound Selol is an organic mixture of selenitetriglycerides, which was previously shown to exhibit antitumor properties. The aim of the present study was to investigate the cytoprotective effect of Selol against sodium nitroprusside (SNP) induced oxidative stress and PC12 cells death. METHODS: The study was carried out using spectrophotometric and spectrofluorometric methods as well as real-time PCR analysis. RESULTS: We found that treatment with SNP (0.5 mM) induced significant elevation of free radicals, decreased the reduced glutathione (GSH) level as well as increased the formation of oxidized glutathione (GSSG). In addition, the significant alteration in the activities of antioxidative enzymes, such as glutathione peroxidase (GPx), glutathione reductase (GR) and thioredoxin reductase (TrxR) were observed after SNP treatment. Selol, at low molecular range neutralized SNP-induced free radicals generation and modulated GSH homeostasis. Moreover, Selol significantly elevated the activities of GPx, GR and TrxR, thus preventing cell death evoked by SNP. The involvement of Selol on the intracellular antioxidative defence system was further confirmed by using a GPx and TrxR inhibitor, sodium aurothiomalate, that abolished its cytoprotective effect. CONCLUSIONS: Taken together, these findings suggest that treatment with Selol protects cells from oxidative stress via enhancement of the intracellular antioxidant potential. The Selol’s efficacy in combating free radical damage suggests that it can be a valuable therapeutic agent in the treatment of neurodegenerative disorders. Supported from MUW FW27/PM34D/14 and MMRC statutory theme 8.
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