Clinical Information

Selenium is an essential element. It is a cofactor required to maintain activity of glutathione peroxidase (GSH-Px), an enzyme that catalyzes the degradation of organic hydroperoxides. The absence of selenium correlates with loss of GSH-Px activity and is associated with damage to cell membranes due to accumulation of free radicals.

The normal daily dietary intake of selenium is 0.01 to 0.04 parts per million (ppm), which is similar to the typical content of soil (0.05 ppm) and sea water (0.09 ppm). Selenium is found in many over-the-counter vitamin preparations because its antioxidant activity is thought to be anticarcinogenic. There is no supporting evidence that selenium suppresses cancer.

In humans, cardiac muscle is the most susceptible to selenium deficiency. With cell membrane damage, normal cells are replaced by fibroblasts. This condition is known as cardiomyopathy and is characterized by an enlarged heart whose muscle is largely replaced by fibrous tissue.

In the United States, selenium deficiency is related to use of total parenteral nutrition. This therapy is administered to patients with no functional bowel, such as after surgical removal of the small and large intestine because of cancer or because of acute inflammatory bowel disease such as Crohn disease. Selenium supplementation to raise the serum concentration to above 70 mcg/L is the usual treatment. Serum monitoring done on a semiannual basis checks the adequacy of supplementation.

Selenium toxicity has been observed in animals when daily intake exceeds 4 ppm. Teratogenic effects are frequently noted in the offspring of animals living in regions where soil content is high in selenium such as south-central South Dakota and northern-coastal regions of California. Selenium toxicity in humans is not known to be a significant problem except in acute overdose cases. Selenium is not classified as a human teratogen.