Selenium (Se)

Deficiency was first identified in experiments in rats,

which were made nutritionally deficient in vitamin E.

The resulting liver injury could be prevented by Se

supplementation.

The optimal range for dietary intake of selenium is

narrow;
Potentially toxic intakes are closer to recommended

dietary intakes than for other dietary trace minerals.

Dietary sources 
selenium-containing amino acids:
seleno-cysteine and
seleno-methionine.
Inorganic forms of selenium are used in supplements.
Seafood, kidney, liver, and meat are good sources
Drinking water usually contains very little selenium
The selenium content of grains and seeds depends on
the selenium content of the soil and the form in which
selenium is present
Metabolism – absorption
Dietary selenium has a high bioavailability (>50%).

Seleno-methionine is actively absorbed in the small

intestine by the methionine absorptive pathway.

The absorptive route of seleno-cysteine is unknown.

Inorganic selenium - passively absorbed / duodenum/.

Selenium absorption appears to be independent of the

individual's selenium status and may be unregulated

Seleno-methionine is incorporated into proteins in place
of methione and serve as a storage pool.
Seleno-cysteine is the active form
absorbed directly from the diet,
synthesized from seleno-methionine, or
synthesized by direct replacement of an oxygen residue
on serine while it is bound to a specific tRNA.
Seleno-cysteine and seleno-methionine are catabolized
to release selenium.
The principal excretory route of selenium is the urine
Biological role
 More than 30 selenoproteins have been identified
Gluthathione peroxidase - antioxidant defense

Iodo-thyronine deiodinase 2 (three forms) - serves as a

catalyst for production of thyroid hormone.

Seleno-protein P and

Seleno-protein synthetase.
Deficiency 
skeletal muscle dysfunction and cardiomyopathy
may also cause mood disorders, impaired immune
function, macrocytosis, and whitened nailbeds.
Keshan disease - an endemic cardiomyopathy that
affects children and women of childbearing age in areas
of China, has been linked to selenium deficiency.
The geographical distribution is associated with local
diets, which are nearly devoid of selenium.
The disorder responds to selenium supplements.
Total parenteral nutrition
 Trace elements added to TPN were historically not
supplemented with selenium.
Several cases of selenium deficiency in chronic TPN users
have been reported with cardiomyopathy and skeletal
muscle dysfunction.
Selenium deficiency has been described in a child with
lymphangiomatosis secondary to loss in chylous fluid
Other clinical effects of selenium deficiency
Immune function
Selenium is found in relatively high amounts in several
tissues with hematopoietic & immune function potential,
including liver, spleen, & lymph nodes.
HIV replication is inhibited by selenium. Studies have shown
a linear relationship between selenium deficiency and a
reduction in CD4 cell counts in HIV-infected patients.
Impaired CMI has been demonstrated when tissue stores of
selenium are depleted.
Nk cell activity is enhanced when selenium is supplemented
in the diet of selenium depleted individuals
Thyroiditis
Selenium supplementation may decrease inflammatory
activity in patients with autoimmune thyroiditis, and
may reduce the risk of postpartum thyroiditis in women
who are positive for thyroid peroxidase (TPO)
antibodies
Cancer — Epidemiologic studies support a possible
relationship between Se and cancer mortality. As a
result, a number of studies have investigated the role
of selenium supplementation for prevention of cancer
Cardiovascular disease
glutathione peroxidase (GPx), a seleno-protein
dependent enzyme, reduces hydrogen peroxide and
other molecules with oxidative potential.
In theory, the antioxidative effect protects lipid
membranes, inhibits oxidative modification of low
density lipoprotein, and suppresses platelet aggregation.
These effects would predict that Se supplementation
should be protective of atherosclerotic disease.
However, prospective and epidemiologic studies have
shown mixed results
Glucose metabolism —
Animal models suggest that low doses of selenium may

improve glucose metabolism, clinical studies in humans

suggest that selenium supplementation does not confer
benefit and may increase the risk of type 2 diabetes.
Dietary reference intake
The RDA for selenium is
 20 mcg daily for young children,
 55 mcg daily for adults