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NOTES ON SELENIUM
Selenium is a mineral trace element, a ‘heavy metal’ with an atomic weight of 79. It is given the number 34 in the Periodic Table and therefore has similarities with Sulphur (above it in the Group), tellurium (below it) and arsenic (in the next group). Since its discovery at the beginning of the 19th century it has been used in many different ways: ceramics, metal alloys, chemical pigments and - more recently - electronics. It is only during the last 30 years that efforts have been made to determine its biological importance and these investigations have led to a much greater understanding of its properties.
The discovery in 1957 that selenium appeared to be an, essential element in the nutrition of animals was not readily accepted. Earlier, Dr. H A Schroeder of the Dartmouth Trace Element Laboratory in USA claimed that he had produced cancer in rats by lifetime feeding of sodium selenate. This one trial, which was never confirmed by subsequent research, led to a decision by the American Food and Drug Administration (FDA) that selenium was a proven carcinogen. Subsequently this concept -was also accepted by the National Academy of Sciences and then by the World Health Organisation. This stigma restricted the widespread study and use of selenium for many years until further extensive studies in the 1960’s failed to produce a single tumour in rats fed sodium selenite or sodium selenate.
The natural source of selenium for agriculture and most other biological uses is the soil from which it is extracted in varying degrees by plants which are subsequently consumed by animals. Soils vary considerably in their selenium contents. Some contain so much selenium that many plants growing thereon are toxic to livestock, whereas other soils have so little that livestock grazing on such pastures become selenium-deficient.
The following scale for determining soil selenium status has been proposed: Soil selenium concentration (mg/kg air-dry soil)
Very high >1.5
High >0.9
Low <0.5
Very low <0.3

Under normal soil conditions, selenium levels below 0.45 mg/kg lead to deficiency conditions in grazing livestock. High levels of Ferric iron in the soil are able to bind selenium so that it is unavailable to plants; thus levels above 0.45 mg/kg are not necessarily adequate.
Levels of selenium in soils appear to be decreasing. The reserves are being drained by increased crop yields and forage growth and by continuous leaching by rain and irrigation water without natural replacement from dead plant tissue or manure. Even the advent of purer, more concentrated fertilisers and the demise of products such as basic slag have affected soil selenium status since the impure fertiliser products often contained traces of selenium.

Research in the mid 1950s showed that certain diseases of livestock which were believed to be caused by deficiencies of vitamin E responded to dietary supplies of selenium. First of all, Schwarz found that liver necrosis of rats fed diets containing torula yeast could be alleviated by a supplement of sodium selenite. Almost simultaneously Patterson and his co-workers found that exudative thathesis of poultry responded to selenium supplementation. A year later (1958) workers at Oregon State University found that white muscle disease of ruminants was similarly selenium—responsive. These conditions had also been shown to respond to vitamin E supplementation. The search was then initiated to find the biochemical pathways in which selenium was involved and the reasons for the similarity of action with vitamin E.
It was not until 1973 that a metabolic role was found for selenium. In that year Rotruck reported that a cell enzyme, glutathione peroxidase (GSH-Px), contained selenium. GSH-Px had been discovered in 1957 in bovine erythrocytes and was shown to be involved in. the removal of active peroxides from cells. It is now known that GSH-Px contains four atoms of selenium per mole of protein of 88,000 molecular weight. Selenium has also been found in some other enzymes in microbial tissue. In most livestock species there is a very close correlation between selenium and GSH-Px levels, suggesting that this is the major site of selenium utilization.

The known role of GSH-Px in controlling cell peroxides enabled Hoekstra to prepare an hypothesis linking the biochemical roles of selenium and vitamin E and explaining their dual function in controlling disease syndromes such as white muscle disease. He suggested that the cause of muscle tissue cell degeneration was the direct chemical action of lipid hydroperoxides. These were formed by the action of active peroxides on unsaturated fatty acids. This could be prevented by two separate actions: the removal of the peroxides by GSH-Px and by the antioxidant activity of tocopherols (vitamin E) in complexing with the unsaturated fatty acids and preventing the formation of hydroperoxides. While this is a belt and braces activity with either action normally being sufficient to prevent hydroperoxide formation, both have to function when cells have heavy loads of active oxygen and/or unsaturated fatty acids.

Selenium also appears to have an independent role in immune responses and additional supplementary selenium has been shown to promote the numbers of 1gM-producing cells and thus the production of 1gM immunoglobulin. This mechanism has not been fully explained.
It is also required to preserve the integrity of the pancreas and thus allow normal fat saponification and digestion, and normal lipid bile salt micelle formation.

A lack of dietary selenium limits the production and function of GSH-Px. This leads to the production of lipid hydroperoxides in cells containing active oxygen with subsequent damage to cell wall tissues. The clinical effects include various forms of myopathy (muscle damage) such as white muscle disease (if skeletal muscles are involved), microangiopathy leading to heart failure (if the heart muscle is involved) or capillary fragility leading to haemorrhage (if the circulatory system is affected); encephalomalacia of young chicks can be related to this effect. Blood vessel permeability can also lead to liver damage followed by necrosis.

Syndromes known to respond to selenium supplementation in the presence of adequate vitamin E include:
Liver necrosis (pig)
Fibrosis of the pancreas (chick)
Exudative diathesis (poultry)
Kidney degeneration (mink, rat)
Nutritional myopathy (ruminants)
Microangiopathy (pigs, calves, lambs)
Gizzard erosion (turkeys)

If too much is given Selenium is toxic when ingested in excessive amounts. Animals grazing seleniferous pasture or given large doses of selenium develop a condition known as blind staggers or a1ka1i disease. This is characterised by loss of hair, sloughing of hooves, lameness, anaemia, excessive salivation, teeth grinding, blindness, paralysis and death. In poultry, egg production and hatchability are reduced and embryo deformities are common including lack of eyes and deformed feet. If the normal nutritional requirement is assumed to be 0.2 ppm, the selenium concentration necessary to induce toxicity symptoms is at least 25 times greater. A dietary concentration of around 5 ppm will induce a chronic toxicity condition in poultry and pigs whereas cattle often tolerate levels which are much higher. Some pastures on seleniferous soils have been shown to contain as much as 25 ppm in the dry matter.

Details have already been given of the very close working relationship between selenium and vitamin E. In practice it has proved very difficult to separate selenium and vitamin E deficiency problems so they tend to be linked together and clinical symptoms treated with both selenium and vitamin E together.
Sulphur can limit the effectiveness of selenium. The two elements are adjacent in the Periodic Table and very similar in their chemical reactions. It has been found that the presence in a feed of excess sulphur can induce selenium-deficiency symptoms. Inorganic sulphur can affect the metabolism of selenium to a greater degree than organic sulphur such as in the sulphur-containing, amino acids.
Arsenic is also closely related to selenium. Cases have been reported where the feeding of organic arsenical products such as arsanilic acid with marginal supplies of selenium has induced symptoms of selenium deficiency. Ferric iron also appears able to bind selenium and make it biologically unavailable.

Most of the selenium found in animals is associated with amino acids or proteins. It is rarely found in organs, tissues or body fluids in inorganic form in more than trace amounts.

The determination of the bioavailability of various forms of selenium is extremely complex because different species appear to vary in their abilities to utilise selenium products, and other products within the feed can affect and alter the bioavailability pattern.

Sodium selenite is generally regarded as the most bioavailability source of selenium and other products are generally compared to it. Sodium selenate is also highly bioavailable but not as good as selenite in most situations (90- 95%). The selenium in protein-bound form in most plant-derived feed products has been shown to have a value 60-- 90% of the selenite Se. The Se in animal products is generally of lower value still in preventing exudative diathesis in poultry. In other species, organic feed sources of Se have been shown to be more effective. Both selenide and elemental selenium are substantially less effective than selenite but can be used to good advantage for slow release products.
Most of the bioavailability studies have compared the effectiveness of different forms of selenium in preventing exudative diathesis in poultry. In a study involving pancreatic fibrosis the selenium in selenomethionine appeared to be four times as available as the Se in selenite, probably due to the ability of the chick pancreas to concentrate selenomethionine. This variability of responses illustrates the impossibility of quoting any standard bioavailability figures for selenium.

Selenium contents of feeds and biological tissues can be determined with a reasonable degree of accuracy by a number of different methods.
The sample has to be prepared carefully to ensure the release of all the selenium from its protein-binding. It is normally digested by a combination of strong acids but care has to be taken to keep the reaction temperature as low as possible because selenium can become volatile as the temperature rises. Once the selenium has been extracted it can be quantified either by a fluorimetric method or by atomic absorption spectrophotometry. The fluorimetric method depends on the reaction of selenium with 2, 3 diaminonaphthalene; the accuracy of the result depends on the efficiency of the sample digestion arid the absence of interfering substances. Selenium cannot be estimated directly by atomic absorption because it does not flame readily. Two methods are currently used to create a quantifiable system. The first is to convert selenium to the hydride which can be estimated as a gas and the other is an electrothermal method using a graphite furnace.
An estimation of selenium status can be made by measuring erythrocyte glutathione peroxidase activity. Since there is a good correlation (see Fig 1) between blood selenium and GSH - Px it is possible to derive a useful indication of the selenium situation by the much simpler determination of GSH - Px. It is even possible to use a spot test which measures by fluorescence the rate of oxidation of
GSH.
The amount of selenium found in feed ingredients is extremely variable and depends particularly on the selenium status of the soil where the crop was grown. Most cereals -Barley, Wheat, Oats, Maize & Rice usually contain between .03 and 0.08 mg/Kg DM. Protein feeds – Soybean meal, Maize gluten, 0.5 and 0.15 mg/Kg DM Grass, Hay and other grass products 0.003 to 0.2 mg/Kg DM.

The requirement for selenium is closely related to the need for vitamin E. However, because selenium is required for glutathione peroxidase, the amount needed is related to the animal’s metabolic rate and the presence in cells of active oxygen (peroxides and superoxides) unlike the vitamin E requirement which is closely linked with the amount of dietary polyunsaturated fatty acids. Selenium needs do not vary with fat intake.
Feeds for any livestock species’ containing less than 0.05 ppm selenium (in the dry matter) are likely to induce symptoms of deficiency, particularly if vitamin E supplies are marginal or the animal is stressed or in a very active metabolic state.
Selenium concentrations between 0.05 - - 0.10 ppm are marginally adequate for farm livestock and unlikely to produce deficiency syndromes. However, such levels may not produce optimum supplies. Sows, for example, have been found to need more than 0.13 ppm in order to decrease prenatal piglet mortality and provide adequate selenium supplies in the milk.
Allowances of selenium should therefore be in excess of 0.1 ppm for all species. Reference to the lists of the selenium contents of feed will show that many cereal-based formulations are unlikely to contain such levels without supplementation. Therefore all feeds for all species should be supplemented with selenium, preferably as sodium selenite. Such supplementation does not, and cannot, take the place of adequate vitamin E supplements.

The suggested level of supplementation for optimum performance in the horse should be in the order of 1.0 to 1.75 mg/500Kg Bodyweight horse per day. This supplementation relies on a contribution of Se from the roughage and other feeds being in the order of 0.3 – 0.5 mg/500Kg Bodyweight horse per day.

Approximate selenium contents
Sodium selenite (Na2SeO3) - 45%
Sodium selenate (Na2SeO4. 10H20) - 20%

The appearance of any vitamin E/selenium deficiency syndromes should be countered by a review of both vitamin E and selenium supplies. Some conditions such as pancreatic fibrosis, exudative diathesis and liver necrosis are most likely to be due to inadequate selenium supplies. Other less specific conditions such as Exertional Myopathies (Rhabdomyolosis & Azoturia) and poor hoof integrity in horses, reduced lambing percentage, poor piglet viability & y and low conception rates might be improved by increasing selenium intakes.