The two faces of selenium.

The nutritionally important trace elements share a high biological activity, implemented through association with enzymes, hormones or vitamins. The same activity responsible for physiological responses at extremely low dietary levels implies the potential for metabolic upset when the elements are ingested at elevated, although still relatively low levels. Selenium provides a classic example of this dichotomy of effects and has generated concerns at both ends of its supply spectrum. Experiences in the Dakotas, mid-19th century, led to identification of toxicity symptoms for which selenium was later shown to be responsible, while separate studies showed that excess selenium was teratogenic in the developing avian fetus. These toxic reactions suggested that selenium might be useful in restricting abnormal cell growth, and recent studies have proved it to be anticarcinogenic in certain specific circumstances. Investigation of selenium's nutrient function has been equally interesting, and when Schwarz showed it to be an essential nutrient in 1957, he began an era of intense research activity. Dietary levels of selenium below 0.02 ppm were found to cause deficiency symptoms affecting muscles, liver and pancreas and glutathione peroxidase was shown to be an active form through which selenium acted to prevent such aberrations. Research continues to seek other active organic combinations for selenium to identify interfering compounds that restrict its bioactivity and to explore biochemical mechanisms involved in its toxicity.