Search

Colloidal selenium, was first used to treat cancer as early as 1911 in both humans and mice. Selenium was identified as the toxic component in forage plants of sheep, cattle, and horses in the 1930s. The animal toxicity of selenium compounds was determined to be from the metabolism by animals of the elevated concentrations of Se-methylselenocysteine and selenomethionine in plants. The metabolism of both Se-methylselenocysteine and selenomethionine by animals gives rise to the metabolite, methylselenide (CH 3 Se-), which if in sufficient concentration oxidizes thiols and generates superoxide and other reactive oxygen species. Cancer cells that may overly express methionine gamma-lyase, or beta-lyase (methioninase), by induced viral genomic expression, are susceptible to free radical-induced apoptosis from selenomethionine or Se-methylselenocysteine supplementation.

Bioavailability and possible benefits of wheat intake naturally enriched with selenium and its products was tested. Wheat obtained by application of an original combination and procedure for foliar supplementation of plants with Se was characterized on the average by five times higher content of Se, the main form being L-(+)-selenomethionine (SeMet). Substitution of Se-deficient wheat by wheat naturally enriched with Se and its products contributed to the increase of daily intake on the average by 18 microg (12-35 microg) in volunteers, which is more than 50% of the average daily intake. Six weeks after the beginning of its application, increased daily intake of Se brought about the increase of its concentration in the plasma of the examined persons by 53%, in their erythrocytes by 37%, in their hair by 44%, and in their urine by 54%. This result was comparable to the effect obtained in the course of an 8-wk daily intake of supplements with 100 microg Se in the form of enriched bakery yeast. Analysis of glutathione peroxidase (GSH-Px) activity in blood, thiobarbituric acid reactive substances (TBARS) in plasma, lipid parameters (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides), and glucose in serum of volunteers showed that the increased Se intake induced increased GSH-Px activity in blood and decreased concentrations of TBARS, lipid parameters, and glucose in blood. Using only one crop (wheat enriched with Se), the existing deficiency of Se in our population can be alleviated. In this way, one-fourth of our population with lower Se intake than 21 microg/d will satisfy basal requirements, whereas one-half will become moderately deficient in Se instead of distinctly deficient in Se.

In vitro 30 min of incubation with selenomethionine (Sm) + vitamin E multiplied by about five platelet selenium (Se) decreased significantly platelet thrombin and ADP-induced aggregation decrease. Four groups of streptozotocin-induced diabetic rats were fed with a supplemented purified diet with an Se-rich yeast (Selenion): DSel, Sm: DSm, Sm alpha-tocopherol: DSmE or unsupplemented diet: D. After 24 wk of supplementation, only a decrease in thrombin-induced aggregation in group DSel compared to DSm and DSmE and D was observed. However, after 24 wk of diet compared to 14 wk, in group D and DSm, a significant increase in thrombin-induced aggregation occurred (p < 0.0001), whereas a significant decrease in groups DSel and DSmE (p < 0.0001, p < 0.03) was noted. After 21 wk of diet, in DSmE, platelet adhesion to fibronectin was significantly decreased compared to group D (p < 0.05). These changes in DSmE were associated with a significant decrease in platelet sorbitol (p < 0.02) and a very significant increase in platelet Se (p < 0.0005). Sm associated with vitamin E would appear more efficient to prevent oxidative damage of diabetic platelet membrane and thus to modulate its hyperactivity.