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Association of selenoprotein S gene polymorphism with ischemic stroke in a Chinese case-control study.

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Previous studies showed that selenoprotein S (SELS) was associated with a range of inflammatory markers, and its gene expression was influenced by a polymorphism in the promoter region. The genetic basis of the ischemic stroke has now been largely determined, so the aim of the study was to examine

Variation in the selenoprotein S gene locus is associated with coronary heart disease and ischemic stroke in two independent Finnish cohorts.

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Selenoprotein S (SEPS1) is a novel candidate gene involved in the regulation of inflammatory response and protection from oxidative damage. This study explored the genetic variation in the SEPS1 locus for an association with CVD as well as with quantitative phenotypes related to obesity and

Association of selenoprotein S gene polymorphism with ischemic stroke: how strong is the evidence?

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Depressed serum selenoprotein P: possible new predicator of increased risk for cerebrovascular events.

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Selenium protection against cellular damage by oxygen radicals is accomplished through selenoproteins. Thus, selenium protection during the development of stroke, an oxidative stress-related disease, may not be appropriately reflected in the total serum selenium concentration. Therefore, we

No association of the -105 promoter polymorphism of the selenoprotein S encoding gene SEPS1 with cerebrovascular disease.

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A common pro-inflammatory promoter variant of the selenoprotein S encoding gene (SEPS1) was studied in young stroke patients from Italy and Germany and in healthy control subjects. The -105A-allele was found in 56 of 205 (27.3%) patients with ischemic stroke IS because of a spontaneous cervical

Selenoprotein T as a new positive inotrope in the goldfish, Carassius auratus.

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Selenoprotein T (SELENOT) is a thioredoxin-like protein, which mediates oxidoreductase functions via its redox active motif Cys-X-X-Sec. In mammals, SELENOT is expressed during ontogenesis and progressively decreases in adult tissues. In the heart, it is re-expressed after ischemia and induces

Hypoxia reduces and redirects selenoprotein biosynthesis.

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Selenium deficiency constitutes a risk factor for the incidence and negative course of severe diseases including sepsis, stroke, autoimmune diseases or cancer. In this study, hypoxia is identified as a powerful stimulus to redirect selenoprotein biosynthesis causing reduced selenoprotein P

Association of a Multigenetic Pro-Inflammatory Profile with Ischaemic Stroke.

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A multigenetic pro-inflammatory profile may increase stroke risk. We investigated whether a higher number of pro-inflammatory genetic variants are associated with ischaemic stroke risk and whether other risk factors further elevate this risk.In a

The metal and metalloprotein profile of human plasma as biomarkers for stroke diagnosis.

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Stroke, a major cause of disability and mortality, affects someone in the United States every 40s. Stroke biomarkers, including those that could be used as a blood test for diagnosis of stroke, have been particularly elusive. We performed a double blind study to identify human plasma biomarkers for

Selenoprotein-P Deficiency Predicts Cardiovascular Disease and Death.

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Selenoprotein-P (SELENOP) is the main carrier of selenium to target organs and reduces tissue oxidative stress both directly and by delivering selenium to protective selenoproteins. We tested if the plasma concentration of SELENOP predicts cardiovascular morbidity and mortality in the primary

Selenoprotein S expression in the rat brain following focal cerebral ischemia.

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Recent studies on cerebral ischemic stroke have demonstrated the importance of the inflammatory response. Ongoing inflammatory insults have been implicated as a secondary mechanism underlying neuronal injury induced by ischemia, and anti-inflammatory strategies have gained considerable interest.

Selenium Drives a Transcriptional Adaptive Program to Block Ferroptosis and Treat Stroke.

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Ferroptosis, a non-apoptotic form of programmed cell death, is triggered by oxidative stress in cancer, heat stress in plants, and hemorrhagic stroke. A homeostatic transcriptional response to ferroptotic stimuli is unknown. We show that neurons respond to ferroptotic stimuli by induction of

Selenium and clinical trials: new therapeutic evidence for multiple diseases.

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The understanding of the essential role of selenium (Se) in human health has increased substantially in recent decades. Micronutrient deficiencies are very common in the general population and may be even more common in patients with different pathologies due to genetic or environmental causes and

Redox Dysregulation in Vascular Pathobiology.

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Oxidation-reduction (redox) reactions comprise a subset of fundamental biochemical reactions found throughout biological systems. While redox reactions are involved in many normal cellular functions, excess oxidative potential, or oxidative stress, can lead to cellular dysfunction and injury.

Ebselen, a useful tool for understanding cellular redox biology and a promising drug candidate for use in human diseases.

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Ebselen is an organoselenium compound with glutathione peroxidase (GPx)-like hydroperoxide reducing activity. Moreover, ebselen has its own unique reactivity, with functions that GPx does not have, since it reacts with many kinds of thiols other than glutathione. Ebselen may affect the thioredoxin

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