Dietary selenium: time to act

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# Dietary selenium: time to act {#article-title-2} The essential trace element, selenium, which we largely obtain from bread and cereals, fish, poultry, and meat, plays a vital part in many metabolic functions. While new research increasingly suggests its relevance to disease prevention, evidence that dietary intake is falling in some parts of the world is giving cause for concern. Selenium is a key component of a number of functional selenoproteins required for normal health. The best known of these are the antioxidant glutathione peroxidase enzymes, which remove hydrogen peroxide and damaging lipid and phospholipid hydroperoxides generated in vivo by free radicals and other oxygen derived species. If not removed, lipid hydroperoxides impair membrane structure and function1 and cause blood clotting disturbances by decreasing the production of prostacyclin while increasing the production of thromboxane.2 Furthermore, lipid hydroperoxides are not stable end products but, in the presence of transition metal ions, can decompose to give further reactive free radicals and cytotoxic aldehydes.3 Such secondary products may initiate more lipid peroxidation, promote atherosclerosis, damage DNA, and metabolically activate carcinogens.3 Selenium also plays an important role in the control of thyroid hormone metabolism. The iodothyronine deiodinases, which are responsible for the conversion of thyroxine (T4) to its active form, triiodothyronine (T3), are selenoenzymes.4 Selenium deficiency may cause reduced growth rates owing to a feedback response which …