Influence of Dietary and Injected Selenium on Whole-body Retention, Route of Excretion, and Tissue Retention of 75SeO32- in the Rat

Burk, Raymond F.; Brown, Daniel G.; Seely, Robert J.; Scaief, Charles C.

doi:10.1093/jn/102.8.1049

Cited by 127 publications

(45 citation statements)

References 11 publications

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“…Treatment of murine hippocampal HT22 cells with sodium selenite resulted in the increased of the level of PGC-1α (peroxisome proliferatoractivated receptor gamma coactivator 1-alpha) and NRF1 (nuclear respiratory factor 1), as well as respiratory chain proteins: cytochrome c and cytochrome c oxidase IV (COX IV). This effect was shown to be independent from antioxidative properties of Se and, in general, lead to improvement of the mitochondrial respiratory rate [24]. The similar effect on mitochondrial level and function was observed in SelH overexpressing HT22 cells [88].…”

Section: Selenium and Selenoproteins In Neuro-logical Disorderssupporting

confidence: 57%

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Selenium in the therapy of neurological diseases. Where is it going?

Dominiak¹,

Wilkaniec²,

Wroczyński³

et al. 2015

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Selenium ( 34 Se), an antioxidant trace element, is an important regulator of brain function. These beneficial properties that Se possesses are attributed to its ability to be incorporated into selenoproteins as an amino acid. Several selenoproteins are expressed in the brain, in which some of them, e.g. glutathione peroxidases (GPxs), thioredoxin reductases (TrxRs) or selenoprotein P (SelP), are strongly involved in antioxidant defence and in maintaining intercellular reducing conditions. Since increased oxidative stress has been implicated in neurological disorders, including Parkinson's disease, Alzheimer's disease, stroke, epilepsy and others, a growing body of evidence suggests that Se depletion followed by decreased activity of Se-dependent enzymes may be important factors connected with those pathologies. Undoubtedly, the remarkable progress that has been made in understanding the biological function of Se in the brain has opened up new potential possibilities for the treatment of neurological diseases by using Se as a potential drug. However, further research in the search for optimal Se donors is necessary in order to achieve an effective and safe therapeutic income.

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Section: Selenium and Selenoproteins In Neuro-logical Disorderssupporting

confidence: 57%

“…[23]. Moreover, selenite can regulate the generation ATP and stabilise the mitochondrial membrane potential [24].…”

Section: Introductionmentioning

confidence: 99%

Selenium in the therapy of neurological diseases. Where is it going?

Dominiak¹,

Wilkaniec²,

Wroczyński³

et al. 2015

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show abstract

“…However, during Se deficiency, the brain shows an ability to preserve this trace element, whereas other organs readily lose Se (13,15,46). In addition, several studies revealed that the regions of human brain enriched for gray matter tend to have higher Se levels, whereas white matter was found to have reduced Se, and Se appeared to concentrate in glandular parts of the brain (41,44,47).…”

Section: Discussionmentioning

confidence: 99%

Comparative Analysis of Selenocysteine Machinery and Selenoproteome Gene Expression in Mouse Brain Identifies Neurons as Key Functional Sites of Selenium in Mammals

Zhang

Zhou

Schweizer

et al. 2008

Journal of Biological Chemistry

164

123

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Although dietary selenium (Se) deficiency results in phenotypes associated with selenoprotein depletion in various organs, the brain is protected from Se loss. To address the basis for the critical role of Se in brain function, we carried out comparative gene expression analyses for the complete selenoproteome and associated biosynthetic factors. Using the Allen Brain Atlas, we evaluated 159 regions of adult mouse brain and provided experimental analyses of selected selenoproteins. All 24 selenoprotein mRNAs were expressed in the mouse brain. Most strikingly, neurons in olfactory bulb, hippocampus, cerebral cortex, and cerebellar cortex were exceptionally rich in selenoprotein gene expression, in particular in GPx4, SelK, SelM, SelW, and Sep15. Over half of the selenoprotein genes were also expressed in the choroid plexus. A unique expression pattern was observed for one of the highly expressed selenoprotein genes, SelP, which we suggest to provide neurons with Se. Cluster analysis of the expression data linked certain selenoproteins and selenocysteine machinery genes and suggested functional linkages among selenoproteins, such as that between SelM and Sep15. Overall, this study suggests that the main functions of selenium in mammals are confined to certain neurons in the brain.

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“…The mechanism that regulates production of excretory metabolites has not been elucidated, but excretion has been shown to be responsible for maintaining selenium homeostasis in the animal (Burk et al, 1972). The excretory metabolites appear in the urine primarily, but when large amounts of selenium are being excreted, the breath also contains volatile metabolites (e.g., dimethylselenide) (McConnell and Portman, 1952).…”

Section: Excretionmentioning

confidence: 99%

Establishment of Dietary Reference Intakes for Dietary Antioxidants

Meyers¹

2000

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Influence of Dietary and Injected Selenium on Whole-body Retention, Route of Excretion, and Tissue Retention of 75SeO32- in the Rat

Cited by 127 publications

References 11 publications

Selenium in the therapy of neurological diseases. Where is it going?

Selenium in the therapy of neurological diseases. Where is it going?

Comparative Analysis of Selenocysteine Machinery and Selenoproteome Gene Expression in Mouse Brain Identifies Neurons as Key Functional Sites of Selenium in Mammals

Establishment of Dietary Reference Intakes for Dietary Antioxidants

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