Abstract
Selenium (Se) has triple faces as an essential, toxic, and pharmacological element. The dose-response relationships of these three characteristics fall in a narrow range. Dietary Se intake levels vary largely between nations and areas, depending on soil and crop Se concentrations. Humans and domestic animals have experienced Se deficiency and poisoning due to low and high Se dietary intake, respectively. In the U.S., Se poisoning among domestic animals occurred in South Dakota, but the north to the central area, including South Dakota, is the main production zone for floor and corn, resulting in higher Se intake among the U.S. population. A part of China and Nordic countries showed low Se intake levels. Most epidemiological studies showing the benefits of Se, including its anticancer effects, have been reported from these areas. The cancer chemoprevention trial by Se supplementation failed to prevent prostate cancer but increased the incidence of diabetes. The anticancer activity of Se could be attributed to its pharmacological activities, which occur at concentrations close to toxic doses, rather than to its antioxidant activities. Se supplementation to Se-deficient humans results in elevated antioxidant enzyme activities. However, after Se-dependent antioxidant activity reaches the plateau level, further Se supplementation would not increase antioxidant activity, and in some cases, it would cause adverse effects of Se, such as diabetes. Misunderstanding these points would cause unnecessary, sometimes harmful, Se supplementation.
