Introduction to Human Nutrition

218 Introduction to Human Nutrition

deposition in various organs. Liver and kidney are the
major target organs when selenium intake is high
but, at lower intakes, the selenium content of the
liver is decreased. Heart and muscle tissue are other
target organs, with the latter, because of its total
bulk, accounting for the greatest proportion of body
selenium. The total body content of selenium can
vary from about 3 mg to 15 mg depending on
dietary intakes.
In the body, dietary selenium can be bound to sele-
nium binding proteins but can also be directly incor-
porated into selenoproteins during translation at the
ribosome complex using a transfer RNA specifi c for
the amino acid selenocysteine; thus, selenocysteine
can be considered as the twenty-fi rst amino acid in
terms of ribosome-mediated protein synthesis.
The major excretion routes of selenium are in urine
(mainly as trimethylselenonium ion), in feces (via
biliary pancreatic and intestinal secretions, together
with unabsorbed dietary selenium), and in breath (as
volatile dimethylselenide). Unlike copper, and partic-
ularly iron, which have ineffi cient excretion mecha-
nisms, selenium is rapidly excreted in the urine. Figure
9.7 gives an overall view of selenium metabolism and
excretion.

Metabolic function and essentiality

Selenocysteine is a component of at least 30 seleno-
proteins, some of which have important enzymic
functions (Table 9.18). Selenocysteine is generally at
the active site of those selenoproteins with catalytic
activity, and functions as a redox center for the
selenium-dependent glutathione peroxidases (cys-
tolic, phospholipid hydroperoxide, extracellular, and
gastrointestinal), iodothyronine deiodinases (types I,
II, and III), and thioredoxin reductases. The glutathi-
one peroxidase isozymes, which account for about
36% of total body selenium, differ in their tissue
expression and map to different chromosomes.

Defi ciency symptoms

Keshan’s disease is a cardiomyopathy that affects chil-
dren and women of child-bearing age and occurs in
areas of China where the soil is defi cient in selenium.
Despite the strong evidence for an etiological role for
selenium in Keshan’s disease (i.e., the occurrence of
the disease only in those regions of China with low
selenium soils and, hence, low amounts of selenium
in the food chain, and only in those individuals with

poor selenium status together with the prevention of

the disease in an at-risk population by supplementa-

tion with selenium), there are certain epidemiological

features of the disease that are not readily explained

solely on the basis of selenium defi ciency. A similar

situation occurs with Kashin–Beck disease, a chronic

osteoarthropathy that most commonly affects growing

children and occurs in parts of Siberian Russia and

in China, where it overlaps with Keshan’s disease.

Although oral supplementation with selenium is

effective in preventing the disease, it is likely that

other factors, apart from selenium defi ciency, are

involved in the etiology of Kashin–Beck disease. There

are also some selenium-responsive conditions with

symptoms similar to Keshan’s disease that occur in

patients receiving total parenteral nutrition.

One explanation for the complex etiology of sele-

nium-responsive diseases in humans is that low

selenium status may predispose to other deleterious

conditions, most notably the increased incidence,

virulence, or disease progression of a number of viral

infections. For example, in a selenium-defi cient

animal model, harmless coxsackie virus can become

virulent and cause myocarditis, not only in the

Selenoproteins

(as selenocysteine)

General body proteins

Selenomethionine

Selenocysteine

Selenite

GS-Se-SG

Selenophosphate GS-SeH

H 2 Se

CH 3 SeH Se-Methyl Sec

(CH 3 ) 2 Se

Selenate

Na 2 SeO 4

breath

(CH 3 ) 3 Se+ urine

Figure 9.7 Selenium metabolism and excretion.