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VetBooks.ir Chapter 33

Selenium

Jeffery O. Hall

INTRODUCTION in humans when added dietary selenium prevented a
cardiomyopathy known as “Keshan disease” (Chen,
Selenium is an essential nutrient that has a relatively
1986). Selenium supplementation may also be protective
narrow window between ingested amounts that result in
against certain types of cancer (Combs, 1997), cardiovas-
deficiencies and those that cause toxicoses. Historically,
cular disease (Duthie et al., 1989) and viral infections
occurrences of livestock disease that mimic clinical pre-
(Schrauzer, 1994; Levander, 2000). Because of the essen-
sentation of chronic selenium poisoning were recorded in
tial nature of selenium, poisoning cases from both natural
the 13th century (Martin, 1973). Marco Polo wrote of plant accumulations of selenium and nutritional overdoses
such cases in western China in 1295. In 1560, Father
are encountered.
Simon Pedro described human cases of presumably
The identified essential functions of selenium are still
chronic selenosis in Columbia (Benavides and Mojica,
increasing. The most notable is GSH, where selenocys-
1965). The first documented record of selenium poisoning
teine is a required component of the enzyme system
in livestock was reported in 1860 by a US Army surgeon
(Brown and Arthur, 2001). Reduced GSH is the primary
(Martin, 1973). T.W. Madison described a fatal disease of
physiologic first defense against free radical damage to
horses that grazed near Fort Randall, South Dakota. It
tissues, helping to maintain functional membrane integ-
also has been speculated that the horse illness that slowed
rity. Several subclasses of GSH are now recognized
General Custer’s Cavalry relief may have been due to
(Cohen and Avissar, 1994; Sunde, 1994). To date, more
selenium, but chronic selenosis generally takes weeks to
than 30 selenoproteins have been identified, many of
develop.
which have vital enzymatic functions (Tiwary, 2004).
Selenium deficiency had been historically linked to a
Thioredoxin reductase I, II, and III (Brown and Arthur,
variety of clinical effects. Since 1949, vitamin E, cysteine 0
2001), 5 triiodothyronine deiodinase (Arthur and Beckett,
and a “factor 3” were known to protect rats from fatal liver
1994) and “selenoprotein” are also selenium dependent.
necrosis (Schwarz and Foltz, 1957). When rats were fed
In addition, selenium plays several roles in normal
torula, a brewer’s yeast, they developed liver necrosis that
immune function, reproductive function, hepatic biotrans-
could be avoided by use of baker’s yeast (Saccharomyces
formation reactions, neurotransmitter turnover, and anti-
sp.). It was postulated that “factor 3,” an essential nutrient,
carcinogenic functions.
was deficient in torula. After much research, the active,
preventive element present in “factor 3” was identified as
selenium. Several metabolic diseases of previously BACKGROUND
unknown origin were later found to relate to selenium defi-
ciency, including “white muscle disease” in calves and Selenium is a member of the nonmetallic elements within
lambs (Muth et al., 1958; Godwin and Fraser, 1966), group VIa of the periodic table. It has an atomic number
hepatosis dietetica in pigs (Eggert et al., 1957), exudative of 34, an atomic weight of 78.96, and has six different
diathesis in poultry (Patterson et al., 1957), and pancreatic naturally occurring stable isotopic masses from 74 to 82
degeneration in poultry (Thompson and Scott, 1969). (Rosman and Taylor, 1997). Selenium has four natural
Since its first discovery as an essential nutrient, sele- oxidation states: 22 (selenides), 0 (elemental), 14 (sele-
nium has been found to act in numerous body systems. In nites), and 16 (selenates) (Barceloux, 1999). Selenium
1973, Se was identified as an essential component of glu- was first identified in 1817 by Jons Jakob Berzelius, a
tathione peroxidase (GSH) enzyme (Flohe et al., 1973; Swedish chemist, who investigated worker illnesses in a
Rotruck et al., 1973). Selenium was shown to be essential sulfuric acid plant at Gripsholm, Sweden (Fredga, 1972).
Veterinary Toxicology. DOI: http://dx.doi.org/10.1016/B978-0-12-811410-0.00033-7
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