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1
Introduction
In 1818, Berzelius in Gripsholm, Sweden, identified selenium as a new
chemical element. From humble beginnings as a residue in a sulfuric acid
vat, selenium has found exciting uses in commerce. Many of these depend
on the remarkable susceptibility of selenium electrons to excitation by
light, resulting in generation of an electric current. This has led to use of
selenium in photoelectric cells, light meters, rectifiers, and xerographic
copying machines. It is also used to decolorize the greenish tint of glass due
to iron impurities or, in excess, to create the ruby-red color seen in warning
signals and automobile tail lights. These and other uses are met by produc-
tion of approximately 266 metric tons of selenium annually in the United
States and worldwide production of 1,559 metric tons (Anonymous, 1979a,
1979b).
The biological significance of selenium was not recognized until it was
identified as the toxic principle causing lameness and death in livestock
grazing certain range plants in the Dakotas and Wyoming (Franke, 1934~.
Dr. Madison (1860) had earlier observed a number of toxicity signs, in-
cluding hair loss, in cavalry horses at Fort Randall in the old Nebraska
Territory. Lameness resulted from inflammation of the feet, followed by
suppuration at the point where the hoof joins the skin and ultimate loss of
the hoof. The consequent tenderness inhibited the search for food and
water, and since no stored forage was available, death was at least partly
attributable to starvation. Similar signs were described by Marco Polo
(Komroff, 1926) in his travels in western China near the borders of Turkes-
tan and Tibet about the year 1295. Loss of hair and nails in humans pre
1
OCR for page 2
2
SELENIUM IN NUTRITION
sumably suffering from chronic selenosis was first described in Colombia
by Father Pedro Simon in 1560.
The discovery in 1957 (Schwarz and Foltz, 1957) that selenium was an
essential nutrient led to an entirely new era of research that continues to-
day. Instead of a primary concern with the toxicity of selenium, nutrition-
ists turned their attention to the metabolic function of this element and the
consequences of its deficiency. Hepatic necrosis in rats, probably associ-
ated with inadequate selenium and vitamin E, was seen by Klaus Schwarz
in 1939 as he used purified diets to study vitamins in Richard Kuhn's labo-
ratory at the Kaiser Wilhelm Institute (now the Max Planck Institute) in
Heidelberg (Schwarz, 1976~. Interestingly, Alvin Moxon, as a graduate
student at South Dakota State University in the early 1930s, documented a
growth response in chicks fed low levels of selenium in a series of studies
designed to explore the toxicity of selenium at graded levels (Oldfield,
1981~. When workers in William Hoekstra's laboratory at the University of
Wisconsin (Rotruck et al., 1973) and Dr. Flohe and his associates (1973) at
Tubingen established the unequivocal relationship between selenium and
glutathione peroxidase, a fundamental connection between this element
and metabolic processes was made. Despite the significance of this find-
ing, it is probable that this is not the only metabolic role that selenium
fulfills. A number of research groups are actively investigating evidence
that other functions exist. These studies and others suggesting a relation-
ship between selenium deficiency and human disease are documented in
the following pages. The reader is invited to peruse them critically, but the
authors would caution that the final chapter for selenium in nutrition has
not yet been written.
Representative terms from entire chapter:
acid vat
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