Micronutrients
Chuong Pham-Huy, Bruno Pham Huy in Food and Lifestyle in Health and Disease, 2022
Selenium (Se) is an essential micro-mineral (metalloid) for human life. Selenium exists as inorganic salts such as sodium selenite or sodium selenate which are often used for the preparation of Se supplements. Selenate is classified as toxic for the organism. In plants and animals, Se often occurs in organic forms such as selenoproteins, selenoenzymes, or amino acids. In humans, Se forms the active site of several antioxidant enzymes including glutathione peroxidase, thioredoxin reductase, iodothyronine deiodinase, formate dehydrogenase, glycine reductase, and so on. It is also present in many selenoproteins, one of which is selenoprotein P. Se is also a component of the amino acids selenomethionine and selenocysteine, in which Se replaces sulfur (S) of methionine and cysteine respectively. Se is required for immune function and for the synthesis of thyroid hormones. At low doses, the health benefits of Se are as an immunomodulator, antioxidant, and anti-carcinogenic. Se also assists enzymes in protecting cell membranes from damage by oxidative stress. During infection, stress, or tissue injury, selenoenzymes can protect cell membranes against the harmful effects of oxidants like hydrogen peroxide (H2O2) or oxygen radicals (3–4, 8, 20–24).
Ultratrace Minerals
Luke R. Bucci in Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
Selenium is found in two basic forms — inorganic and organic. Inorganic selenium is encountered as water-soluble selenites () and selenates () found in water supplies.1054 Organic selenium is found as selenomethionine and selenocysteine in plant and animal foods. Selenomethionine is the major organic form of selenium in the diet. Selenomethionine is the major storage form of selenium in the body and is converted to selenocysteine in a highly regulated manner for inclusion into GPx enzymes. Selenocysteine can also be produced from inorganic sources. At present, supplemental forms of selenium include sodium selenite, sodium selenate, selenomethionine, and selenium-enriched yeast.
Treatment and Pharmacological Interventions in Streptozotocin Diabetes
John H. McNeill in Experimental Models of Diabetes, 2018
In vivo insulin-like effects of selenate were reported in 1991 by McNeill et al.43 using STZ diabetic Wistar rats. The rats were treated with sodium selenate, administered i.p. daily for 8 weeks at doses ranging from 10 to 15 μmoles/kg. The selenium-treated diabetic rats had partially improved blood glucose levels without an increase in plasma insulin levels. Food and fluid intakes, which were elevated in the diabetic rats, were partially restored to normal due to the treatment. In addition to the improvement in plasma glucose levels, improvements in integrated glucose response to both oral and i.v. administration of glucose were seen when selenate (16.5 μmol/kg) was administered orally.44 Battell et al.45 reported that selenate administered i.p. was able to improve heart function in STZ diabetic rats.
Targeting the Wnt/β-catenin pathway in neurodegenerative diseases: recent approaches and current challenges
Published in Expert Opinion on Drug Discovery, 2020
Annalucia Serafino, Daniela Giovannini, Simona Rossi, Mauro Cozzolino
Selenium is an essential trace element vital for brain, involved in various functions of the CNS, including memory and cognition, and which deficiency has been reported to be associated with the pathophysiology of neurodegenerative disorders including AD, PD, ALS, and epilepsy [148]. There is increasing evidence that selenium dietary intake is inversely associated with the mortality in AD patients [149]. Selenium has multiple biological functions via different selenoproteins [148]. Compared with other selenium compounds, sodium selenate substantially promotes phosphatase activity by acting as a specific agonist for protein phosphatases of type 2A (PP2A) [150], a heterotrimeric serine-threonine phosphatase that controls a variety of cellular events via protein dephosphorylation. Among its different functions, PP2A is also responsible for dephosphorylation of inactive β-catenin and phosphorylated APP [151,152]. It has been demonstrated in a mouse model of AD that sodium selenate is able to significantly promote the activity of PP2A and repress the hallmarks of the disease [153]. Specifically, the activation of PP2A by sodium selenate led to the activation of Wnt/β-catenin signaling by increasing β-catenin level and inhibiting GSK-3β activity (Figure 2 and Table 1). Concomitantly, in selenate-treated animals the phosphorylation levels of APP were also reduced, leading to decreased APP cleavage and Aβ plaque production [153].
Comparative study of radioprotective effects of selenium nanoparticles and sodium selenite in irradiation-induced nephropathy of mice model
Published in International Journal of Radiation Biology, 2018
Masoumeh Karami, Siamak Asri-Rezaei, Banafshe Dormanesh, Ali Nazarizadeh
Although Se was identified as essential to human nutrition more than 50 years ago, its daily requirement still needs to be elucidated (Brown and Arthur 2001). Despite its crucial roles in human and animals health, low margin of safety is a concerning issue. Protective effects of Se in animals usually occur at 1–3 μg Se/g diet; however, the toxicity threshold is 3–5 μg Se/g diet (Ip and Ganther 1990; Maier and Knight 1994). Furthermore, there is almost no survival of rats fed 16 μg Se/g diet (Wang et al. 2007). The antioxidant and pro-oxidant effects or bioavailability and toxicity of Se depend on its chemical form (Wang et al. 2007). A number of dietary supplements of Se such as sodium selenite (Na2SeO3) or sodium selenate (Na2SeO4) and Se-enriched yeast (SY) are currently available in commercial marketing. However, high toxicity and low biosafety of the available supplements is a limiting factor.
New discoveries in progressive myoclonus epilepsies: a clinical outlook
Published in Expert Review of Neurotherapeutics, 2018
Shweta Bhat, Subramaniam Ganesh
Invariably in all the PMEs neurodegeneration at the molecular level is the hallmark feature. Oxidative stress is the major predisposing factor for neurodegeneration and epilepsy. Therefore, antioxidants have long been used in the management of PMEs. N-acetylcysteine (NAC), riboflavin, vitamin E, selenium, and zinc were shown to be useful in case of ULD [146]. Cofactors and vitamins with antioxidant properties namely coenzyme Q10 (CoQ10), L-carnitine, hydroxy-L-tryptophan are used in combination with idebenone (150 mg × 3 daily) in managing MERRF [123,128]. In addition, antioxidant sodium selenate has been reported to reduce seizure sensitivity in LD mouse model [147]. The ketogenic diet (2:1 to 4:1 fat to carbohydrate and protein) is yet another non-pharmacological treatment approach in controlling refractory epilepsy, but improvement in PMEs is limited [123,128,148]. Combinatorial therapy using antioxidants, such as vitamin E, Resveratrol, selenium, curcumin, and some chemical chaperones, such as trimethylamine N-oxide dihydride (TMAO) was reported in the management of NCL [149]. Omega 3/6 fatty acids were reported to exert protective effects in neuronal cells from mice deficient for Ppt1 (NCL1 model).
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