Selenium

General Information

Selenium is an essential trace element which has, however, a low threshold of toxicity commencing at approximately ten times the dietary requirement.

Selenium is present at the active site of two enzymes, Glutathione peroxidase and Type 1 iodo-thyronine 5'-deiodinase. Glutathione peroxidase, which is found as distinct intracellular and extracellular variants, catalyses in vitrothe destruction of hydrogen peroxide and organic hydroperoxides. Type 1 iodo-thyronine 5'-deiodinase, present mainly in liver and kidney, mediates conversion of thyroxine (T4) to 3,3'-triiodothyronine (T3). An additional extracellular Se-containing protein, selenoprotein-P, accounts for approximately 50% of human plasma selenium; its function is unknown.

Deficiency:

Outside China, where two diseases (Keshan Syndrome and Kashin-Beck Disease) which are related to selenium deficiency, symptomatic selenium deficiency in humans appears to be restricted to patients on parenteral nutrition and children with inborn errors of metabolism who require very specialised diets.Therefore, laboratory investigation of selenium deficiency should be restricted to the monitoring of patients receiving parenteral nutrition and other medically indicated diets, or the investigation of conditions arising from malnutrition or exotic dietary habits.

 In clinical practice selenium is usually measured in plasma (or serum), providing an index of recent intake of the element. However, plasma selenium has recently been shown to possibly be an acute-phase reactant, in which case the lowered concentration may be the result of tissue redistribution rather than a nutritional deficit. In this circumstance, an acute phase response should be confirmed by measurement of C-reactive protein.

Toxicity:

Selenium is used in the electronics industry and in the manufacture of shampoos, paints, dyes and glass. Smelting and refining processes may result in exposure to fumes of elemental selenium and selenium dioxide, in addition to hydrogen selenide. Acute symptoms described include intense irritation of eyes, nose, mouth and lungs, chronic exposure producing, in addition, “garlic breath”, nausea and anorexia.
Self-poisoning, accidental and deliberate, has occurred by ingestion of selenious acid alone, or more frequently, in combination with copper nitrate and nitric acid, as gun-blueing compound. This substance was implicated in the UK in an attempted criminal poisoning; the symptoms exhibited by the victim were consistent with chronic selenosis.
Following acute ingestion, symptoms described include gastrointestinal upset, abdominal pain, agitation, altered consciousness level and cardio-respiratory arrest. In such cases the contribution of the element alone to the poisoning is difficult to assess in view of the fact that solutions containing selenium may be quite strongly acidic.

In cases of known acute selenium poisoning, measurement of serum or plasma selenium concentration will confirm ingestion and degree of absorption, but may not provide a reliable indication of the severity of poisoning or a guide to prognosis. It is however, a good indicator of excessive chronic ingestion, but again may not reflect symptomatology.