Chemistry Reference
In-Depth Information
CHAPTER
38
Selenium
JOHAN HÖGBERG AND JAN ALEXANDER
ABSTRACT
The LD
50
ranges between 1.5 and 6 mg/kg body
weight (bw) for many selenium compounds and ani-
mal species. The central nervous system (CNS) seems
to be the target organ at these dose levels, but the liver,
heart, and lungs may also be affected. Cases of acute
selenium poisoning in humans have been described,
a few with fatal outcomes. These cases occurred either
after consumption of selenium or after exposure
through inhalation. Gastrointestinal and neurological
symptoms predominated.
Chronic poisoning caused by long-term exposure has
been reported in livestock and humans from geographi-
cal areas where soil contains high levels of selenium.
In rodents, liver cirrhosis is a common effect, whereas
typical effects in domestic animals are emaciation,
deformation of hooves, loss of hair, and joint erosions.
In humans consuming 1-5 mg Se/day, hair and nail
problems have been reported and are very common at
5 mg Se/day. An intake of approximately 1200
Selenium is an essential trace element and has been
shown to be a natural component in the enzymes
glutathione peroxidases (GSH-px 1-5), iodothyrodine
deiodinases, thioredoxin reductases, selenoprotein P, and
other proteins, altogether 25 proteins. Most selenium
inorganic and low molecular compounds are water
soluble and can effi ciently be taken up in the intestine.
Soluble, as well as nonsoluble, compounds can be taken
up by the lungs. Selenium occurs as cysteine in seleno-
proteins, whereas selenomethionine can unspecifi cally
substitute for methionine in proteins. The selenium
requirement to compensate minimal losses in man is
50-70
g/day.
When given in excess, selenium compounds are
rapidly distributed to major organs of the body. In the
liver, many selenium compounds are biotransformed
to excretable metabolites. Identifi ed metabolites include
selenosugars in urine and dimethylselenide in breath.
Biotransformation seems to be a major mechanism by
which selenium homeostasis is maintained during
excessive exposure, and there is a rapid phase and a
slow phase of elimination. The half-life of the rapid
phase is 1-3 days, depending on the compound ingest-
ed, and for the slow phase it is 30-110 days.
Blood levels are approximately 0.027
µ
µ
g/day
is the LOAEL for clinical selenosis, and 850
g/day
can be taken as a NOAEL for clinical selenosis. How-
ever, a clinically insignifi cant rise of serum ALAT has
been reported at slightly lower doses. Other adverse
effects among few individuals in larger study cohorts
have also been reported at lower doses. Skin lesions
and depigmentation are also common signs of intoxi-
cation. In more severe cases, neurological and gastroin-
testinal symptoms predominate. Death, albeit rarely,
has been associated with chronic selenium poisoning.
Although several selenium compounds have been
tested for possible carcinogenic potential, only selenium
sulfi de in large oral doses has shown convincing carcino-
genic effect. On the contrary, some of these compounds
have been shown to prevent the development of cancer.
µ
g/mL in
geographical areas with low selenium intake, and
an intake of about 90
µ
µ
g/day would correspond to
approximately 0.11
g/mL. Toxic effects have been
seen at blood levels ranging from 0.179-7.5
µ
g/mL.
In most parts of the world, normal urine levels are
0.03 mg/L. Occupationally exposed workers usually
excrete < 0.l
µ
µ
g/mL.
