Abstract
Selol is an organic selenitetriglyceride formulation containing selenium at +4 oxidation level that can be effectively incorporated into catalytic sites of of Se-dependent antioxidants. In the present study, the potential antioxidative and cytoprotective effects of Selol against sodium nitroprusside (SNP)-evoked oxidative/nitrosative stress were investigated in PC12 cells and the underlying mechanisms analyzed. Spectrophoto- and spectrofluorimetic methods as well as fluorescence microscopy were used in this study; mRNA expression was quantified by real-time PCR. Selol dose-dependently improved the survival and decreased the percentage of apoptosis in PC12 cells exposed to SNP. To determine the mechanism of this protective action, the effect of Selol on free radical generation and on antioxidative potential was evaluated. Selol offered significant protection against the elevation of reactive oxidative species (ROS) evoked by SNP. Moreover, this compound restored glutathione homeostasis by ameliorating the SNP-evoked disturbance of GSH/GSSG ratio. The protective effect exerted by Selol was associated with the prevention of SNP-mediated down-regulation of antioxidative enzymes: glutathione peroxidase (Se-GPx), glutathione reductase (GR), and thioredoxin reductase (TrxR). Finally, GPx inhibition significantly abolished the cytoprotective effect of Selol. In conclusion, these results suggest that Selol effectively protected PC12 cells against SNP-induced oxidative damage and death by adjusting free radical levels and antioxidant system, and suppressing apoptosis. Selol could be successfully used in the treatments of diseases that involve oxidative stress and resulting apoptosis.
Highlights
Selenium (Se) is an essential trace element that is biologically active in the form of Se-containing selenoproteins
In order to determine if Selol might influence the oxidative/nitrosative stress evoked by sodium nitroprusside (SNP), we evaluated the effect of Selol on SNP-induced reactive oxygen species (ROS) accumulation
PC12 cells serve as a common model for the investigation of neurotoxic effects of stress [38] as well as neuroprotection induced by candidate drugs [39]
Summary
Selenium (Se) is an essential trace element that is biologically active in the form of Se-containing selenoproteins. This mineral when replaced the sulfur atom in the amino acid cysteine (Cys) forms selenocysteine (Sec), which is the 21st proteinogenic amino acid. Brain is vulnerable to oxidative stress due to its high oxygen demand (it takes up to 20 % of the total oxygen consumed), high levels of iron and unsaturated fatty acids along with relatively inefficient antioxidative defense [1]. Oxidative stress plays an important role in brain aging as well as in various neurodegenerative diseases [2, 3] along with the deregulation of nitric oxide (NO)-based signaling, neurotransmission, and immune function [4]. The association between the risk of neurodegenerative diseases and the antioxidative capacity has been demonstrated by numerous studies, suggesting
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