Selenium [Se, 34]
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42.6 HUMANS
Selenium content of normal adult humans can vary widely. Values from 3 mg in New
Zealanders to 14 mg in some Americans reflect the profound influence of the natural
environment on the Se contents of soils, crops, and human tissues. Approximately
30% of tissue Se is contained in the liver, 15% in the kidney, 30% in the muscle, and
10% in the blood plasma (WHO 2004). The average Se contents in the blood are
within the range of 40–400 μg/L (Gać and Pawlas 2011). Selenium can also be found
in significant amounts in the nails and hair. Approximately 50%–80% of absorbed Se
is eliminated in the urine.
Following ingestion, most water-soluble inorganic and organic Se compounds in
foods are relatively efficiently absorbed across the gastrointestinal tract (80%–95%),
although elemental Se and Se sulfide are poorly absorbed. A number of other factors
besides chemical forms may also influence the bioavailability and distribution of Se
(Thomson 1998). Organic forms (e.g., selenoamino acids such as selenomethionine
and selenocysteine) are absorbed more readily than inorganic forms, as well as on
the overall exposure level, with absorption increasing, when Se levels in the body
are low.
The nutritionally essential functions of Se appear to be discharged by some 25
selenoproteins. The specific selenoproteins include glutathione peroxidases (it is a constituent element of the entire defense system that protects the living organism from the
harmful action of free radicals), thioredoxin reductases, 5-iodothyronine deiodinases,
selenoprotein P, and others. Many forms of Se (including selenite, selenate, selenocysteine, and selenomethionine) are metabolized to hydrogen selenide. While the latter
metabolite is the obligate precursor to the formation of selenocysteine in the specific
selenoproteins, it can also be serially methylated (to methyl selenol, dimethylselenide,
and trimethylselenonium ion) or converted to a selenosugar, and excreted.
Selenium aids in the defense of oxidative stress, the regulation of thyroid hormone
action, and the regulation of the redox status of vitamin C and other molecules. Its
activity appears to be closely related to the antioxidative properties of α-tocopherol
(vitamin E) and coenzyme Q (ubiquinone). Organic and inorganic Se compounds
function is in preventing certain disease that have been, in the past, associated with
vitamin E deficiency. Selenium protects the organism from oxidative damage to cell
membranes by destroying H 2 O 2 , whereas vitamin E protects against damage by preventing the formation of the lipid hydroperoxides.
Selenium role in aging processes and prevention of age-related diseases depends
upon a complex combination of Se status, Se bioavailability, genetic variations in
selenoprotein genes, and the regulation of downstream metabolic pathways involved
in the aging process.
Selenium inadequacy is common in older people. In particular, it was reported
that Se intake is reduced in elderly people and that Se status declines in an agedependent manner. The Epidemiology of Vascular Ageing study established a relationship between Se status and longevity. Significantly higher mortality in people
with low plasma Se, and an association between plasma Se concentration and mortality by cancer, suggests that inadequate Se intake may increase the vulnerability to
diseases (Méplan 2011).