Selenium serum supplement

The possible involvement of free radicals in the development of hypertension has been suspected for a long time. In 1988, Salonen et al. [73] demonstrated the marked elevation of blood pressure for persons with the lowest levels of plasma ascorbic acid and serum selenium concentrations. In subsequent studies these authors confirmed their first observations and showed that the supplementation with antioxidant combination of ascorbic acid, selenium, vitamin E, and carotene resulted in a significant decrease in diastonic blood pressure [74] and enhanced the resistance of atherogenic lipoproteins in human plasma to oxidative stress [75]. Kristal et al. [76] demonstrated that hypertention is accompanied by priming of PMNs although the enhancement of superoxide release was not correlated with the levels of blood pressure. Russo et al. [77] showed that essential hypertension patients are characterized by higher MDA levels and decreased SOD activities. 

For suspension cultures, the concentration of calcium and magnesium should be kept low to prevent cell aggregation and adhesion. Other metals, such as iron, manganese, selenium, vanadium, zinc, copper, and molybdenum, are usually added to the culture medium, but at reduced concentrations, and mainly if the medium is not supplemented with animal serum. 

A serum-free medium supplemented with insulin, transferrin, ethanolamine and selenium (ITES) allows growth of certain hy-bridomas at 17-74% the rate found with 15% FBS (Wolpe, 1984) and Cleveland et al. (1983) devised a protein-free medium for growth of myeloma cells which, with addition of BSA at 2.5 mg/ml, forms the basis of Costar s SF-1 and SF-X supplemented media. Cloning is still very difficult in serum-free media, but feeder layers can be replaced by culture supernatants from human endothelial cells (HECS Astaldi, 1983) or Ewing s sarcoma cells (ESG Ley et al., 1980) — see 5.8.5. 

Kolacz, R., Dobrzanski, Z., and Grudnik, T. 2001. Effect of selenium yeast feed supplement on selenium level in sow milk and piglet blood serum and on production performance. Folia Univ. Agric. Stetinensis 224, 77-81. 

Some practitioners advocate withholding trace elements from CKD and ESKD patients receiving PN. There are no published guidelines specific for the use of trace elements in these patients. Because serum concentrations in ESKD patients of certain trace elements are normal (e.g., manganese) and others are decreased (e.g., zinc and selenium), the standard dietary intake of these trace elements is recommended, and standard trace element supplements should be added to PN regimens. Additional zinc and selenium supplementation may be considered in documented cases of deficiency. 

Selenium supplementation has been shown to affect type-I-deiodinase activity in male rats (Behne et al. 1992 Eder et al. 1995 Hotz et al. 1997). Exposure to 0.055 or 0.27 mg selenium/kg/day as sodium selenite in food for 40 days produced a significant decrease (approximately 50%) in serum levels of T3 and a nonsignificant reduction in type-I-deiodinase activity compared with rats receiving 0.009 or 0.026 mg selenium/kg/day (Eder et al. 1995). Exposure to 0.27 mg selenium/kg/day did not produce any other adverse signs, such as weight loss or decreased food consumption, and serum T4 levels were similar in all groups. 

Selenium is a component of all three members of the deiodinase enzyme family, the enzymes responsible for deiodination of the thyroid hormones (Kohrle 1994 St. Germain and Galton 1997). The deiodinases contain a selenocysteine at the active site, which is required for catalytic activity. There are three types of deiodinases and they differ in terms of tissue distribution, reaction kinetics, efficiency of substrate utilization, and sensitivity to inhibitors. The first to be recognized as a selenoprotein was type I iodothyronine 5 -deiodinase which converts the prohormone thyroxine (T4) to the active form, triiodothyronine (T3) and to date, studies of the effects of excess selenium have focused on this protein. Under normal circumstances the human thyroid produces only 20-30% of its hormone as T3 the remainder is T4 (a minute amount of reverse T3 (rT3) is also produced), which is largely converted to active T3 by type I deiodinase located within the liver, euthyroid pituitary, kidney, thyroid, and brain. Type I deiodinase is a membrane bound protein and, thus, its activity has not been directly measured in studies of humans supplemented with selenium. Human studies have instead measured serum levels of T3, rT3, T4, and TSH. 

Meltzer HM, Norheim G, Loken EB, et al. 1992. Supplementation with wheat selenium induces a dose-dependent response in serum and urine of a Se-replete population. Br J Nutr 67(2) 287-294. 

A twelve-month selenium-supplementation trial in children with KBD in Tibet did not show any effect on the main symptoms and signs of the disease (Moreno-Reyes et al., 2003). But, in the same study, correction of iodine deficiency before the administration of selenium supplements induced partial recovery of growth retardation. Selenium had no additional effect on either growth or thyroid function, despite the normalization of serum-selenium levels. 

In KBD subjects, the evolution of thyroid function after correction of iodine was similar in selenium supplemented and nonsupplemented subjects. This finding corroborated previous studies, suggesting only a moderate effect of selenium deficiency on thyroid hormones in human (Calomme et al, 1995 St. Germain and Galton, 1997). In Tibet, the administration of an intramuscular injection of 475-mg of iodine to KBD subjects was sufficient to correct iodine deficiency for 16 months, because at this time serum T3 increased again to pre-iodine levels and mean iodine urinary concentrations had fallen... 

For further work, serum has been replaced by insulin and transferrin, and a routine assay for retinoids in serum-free medium is performed as follows (Breitman et al., 1980a) HL-60 cells are seeded at a density of 2 x 10 cells per ml in defined medium, which is a 1 1 mixture of Dulbecco s modified Eagle s minimum essential medium and Ham s F-12 medium supplemented with 3 x 10 M selenium dioxide, insulin (5 xg per ml), and transferrin (5 ig per ml). Retinoids are added to the HL-60 cells at the start of the assay, using ethanol as the vehicle final concentration of ethanol does not exceed 0.1%. The cells are incubated for 4 or 5 days, and differentiation is then measured by NBT reduction (Collins et al., 1979) of cytospin slide preparations. Results are expressed as percentage of NBT positive cells. Approximately 4-8% of the cells will differentiate spontaneously in the absence of added retinoid. As with the F9 system, dose-response curves have been determined for a large number of retinoids, and some of the more significant results are shown in Table III. 

The NCI-N87 cells were maintained in DMEM/F12 medium supplemented with 10% FBS, 100 units/ml penicillin and 100 pg/mL streptomycin in a CO2 incubator (5% CO2 and 95% air, 37 C). The cells (5x104 cells/1 mL/well) were incubated in a 12-well plate for 24 hrs, followed by replacing the DMEM/F12 medium with serum-free DMEM/F12 medium (SFM) containing 5 pg/mL transferrin and 5 ng/mL selenium. Twenty-fom hours later, the medium was replaced again with SFM alone or SFM containing each CLA isomer or linoleic acid, a positive control agent, at a concentration of 20 pM. The incubation was continued over a period of 6 days. The number of cells was determined every two days by MIT assay 19). 

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