On the nature of selenium toxicity and carcinostatic activity.

Our objective was to determine the effect of level and chemical form of dietary selenium on productivity of beef cows, concentrations of triiodothyronine (T3), and thyroxine (T4) in plasma, and immunoglobulins (IgG and IgM) in plasma and colostrum of cows. Pregnant cows (n = 60) were randomly allocated among four dietary treatments of 20, 60, or 120 ppm Se as selenite and 60 ppm as selenomethionine from selenized yeast (SeY) in salts offered free-choice. Treatments began 90 d prepartum and continued through the second parturition. Treatments did not affect the final body weights of cows or birth weights or weaning weights of calves. At parturition, cows given salt with 20 ppm Se as selenite had lower (P < . 05) concentrations of Se in blood than cows with access to higher-Se salts. Treatments affected (P < .01) the concentration of T3 and the ratio of T3:T4 in plasma of cows. The concentration of T3 in plasma of cows with access to salt with 20 ppm Se was 14% lower than that in cows supplemented with 60 ppm Se as selenite or SeY. Plasma IgG in cows and calves, colostrum, and Se concentrations in colostrum, casein, and whey were lowest (P < .01) for cows given salt with only 20 ppm Se. Thus, salts with concentrations of 60 and 120 ppm Se improved measures of Se status in cows and calves. Consideration should be given to the concentrations of T3 and IgG when determining the nutritional requirements for Se in cattle.

Effect of level and source of dietary selenium on concentrations of thyroid hormones and immunoglobulins in beef cows and calves.

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New metabolic roles for selenium.

Effects of prenatal source and level of dietary selenium on passive immunity and thermometabolism of newborn lambs.

Selenium (Se) is an essential micronutrient for humans, acting as a component of the unusual amino acids, selenocysteine (Se-Cys) and selenomethionine (Se-Met). Where Se levels are low, the cell cannot synthesise selenoproteins, although some selenoproteins and some tissues are prioritised over others. Characterised functions of known selenoproteins, include selenium transport (selenoprotein P), antioxidant/redox properties (glutathione peroxidases (GPxs), thioredoxin reductases and selenoprotein P) and anti-inflammatory properties (selenoprotein S and GPx4). Various forms of Se are consumed as part of a normal diet, or as a dietary supplement. Supplementation of tissue culture media, animal or human diets with moderate levels of certain Se compounds may protect against the formation of DNA adducts, DNA or chromosome breakage, and chromosome gain or loss. Protective effects have also been shown on mitochondrial DNA, and on telomere length and function. Some of the effects of Se compounds on gene expression may relate to modulation of DNA methylation or inhibition of histone deacetylation. Despite a large number of positive effects of selenium and selenoproteins in various model systems, there have now been some human clinical trials that have shown adverse effects of Se supplementation, according to various endpoints. Too much Se is as harmful as too little, with animal models showing a "U"-shaped efficacy curve. Current recommended daily allowances differ among countries, but are generally based on the amount of Se necessary to saturate GPx enzymes. However, increasing evidence suggests that other enzymes may be more important than GPx for Se action, that optimal levels may depend upon the form of Se being ingested, and vary according to genotype. New paradigms, possibly involving nutrigenomic tools, will be necessary to optimise the forms and levels of Se desirable for maximum protection of genomic stability in all humans.

Selenium and its' role in the maintenance of genomic stability.

Selenium deficiency in rats for a period of up to 6 weeks inhibited both the production of 3,3',5-tri-iodothyronine (T3) from thyroxine (T4) (5'-deiodination) and also the catabolism of T3 to 3,3'-di-iodothyronine (5-deiodination) in liver homogenates. The hepatic stores of T3 were decreased by only 8% in selenium deficiency, despite the T3 production rate from T4 being only 7% of the rate found in selenium-supplemented rats. Hepatic glutathione S-transferase (GST) activity was increased in both hypothyroidism and selenium deficiency, but apparently by different mechanisms, since mRNA expression for this family of enzymes was lowered by hypothyroidism and increased in selenium deficiency. It is concluded that, since both T3 production and catabolism are inhibited by selenium deficiency, there is little change in hepatic T3 stores, and therefore the changes in the activity of certain hepatic enzymes, such as GST, that are found in selenium deficiency are not the result of tissue hypothyroidism.

A Russell

Papers

Effect of selenium deficiency on hepatic type I 5-iodothyronine deiodinase activity and hepatic thyroid hormone levels in the rat.