Selenium is a
non-metal element that is found in the oxygen series and exists
in multiple oxidation states (i.e. -2, +4, +6). Within biological
systems, the element is a constituent of the amino acids that
compromise proteins. The element was first studied around 1930
after scientists noted that cows grazing on plants growing in
high-selenium soil suffered from alkali disease. Studies linking
nutritional diseases to selenium deficiency in sheep, cattle,
and swine continued until 1973 when the biochemical function
of the element was discovered. Researchers discovered that selenium
was an essential component of the glutathione peroxidase enzyme
system (5). The importance of selenium in the human diet was
discovered in 1979. Chinese scientists showed that children living
in selenium-deficient areas were suffering from a cardiomyopathy
known as Keshan disease. The symptoms of the disease were reversed
when selenium was added to the diet. These discoveries led to
expansive research investigating further unknown roles of selenium
within the human body. The massive influx of selenium research
led to the establishment of dietary recommendations from the
World Health Organization (WHO). In accordance with the WHO,
a Recommended Daily Allowance (RDA) was established for the element
in 1989 (5,13)
of food varies widely between regions throughout the world. Plants
acquire selenium from the soil and therefore vary in content
depending upon the region they are grown in (13). Some fruits
and vegetables also appear to lack a growth-dependence on selenium
and in turn have a low content of the mineral regardless of the
soil content. Because of the great variance in selenium soil
and plant content, tables providing selenium content of foods
are difficult to establish. Despite this, some foods are known
to be generally high in selenium content. In general animal products,
especially organ meats, are greater in selenium content than
plant sources (5,13). A common practice in countries where the
soil is poor in selenium is the addition of sodium selenite (Na2SeO3)
to the feed of animals. Seafood, except some fish, is believed
to be the best source of selenium. Mercury compounds found in
some fish bind the selenium thereby making it unavailable to
humans. However, some speculate that the selenium content of
fish containing only traces of mercury is also low (13). Animal
sources of selenium also appear to be higher due to a greater
homeostatic control of the element during a wide variety of exposure
of selenium enter the body as part of amino acids within proteins.
The two most common forms of the element that enter the body
are selenomethionine and selenocysteine which are found mainly
in plants and animals respectively (5). The primary sites of
absorption are from throughout the duodenum. Virtually no absorption
occurs in the stomach and very little takes place in the remaining
two segments of the small intestine (13). Selenomethionine is
absorbed from the duodenum at a rate close to 100%. Other forms
of the element have been shown to also be generally well absorbed.
However, absorption of inorganic forms of the element varies
widely due to luminal factors (5). This variation in absorption
reduces total absorption of all forms to somewhere between 50
and 100%. Selenium absorption is not affected by body selenium
status. Absorption of selenium is closely related to multiple
nutritional factors that inhibit or promote absorption. Vitamins
A, C, and E along with reduced glutathione enhance absorption
of the element. In contrast, heavy metals (i.e. mercury) decrease
absorption via precipitation and chelation (13).
The exact mechanisms
of selenium transport are thus far unclear and debatable. Some
aspects of selenium transport are better understood than others.
For example, selenium has been hypothesized to enter red blood
cells via diffusion and carried throughout the body. Within the
blood, free selenium binds to lipoproteins such as VLDL or LDL.
The transport properties of a second protein, identified as selenoprotein
P, have been met with opposing viewpoints. The protein is found
in the plasma and is believed to be a carrier by some (13). Others
believe that the presence of selenocysteine within the structure
inhibits the transport abilities of the protein (5). To complicate
things even further, the mechanism of selenium release from transport
proteins is very vague.
is absorbed becomes a part of both transport and storage proteins.
Selenium is believed to influence the formation of the proteins.
The uptake of selenium is a complex process that involves numerous
factors. The heart, kidney, lung, liver, pancreas, and muscle
contain very high levels of selenium as a component of glutathione
(5,13). In addition, type I (slow twitch) muscle likely contains
greater amounts of reduced glutathione than Type IIb (fast twitch)
because of their oxidative capacity. The liver is a major supplier
of circulating reduced glutathione, which is reflected in the
amount of its reserves. The volume of glutathione in the liver
is from 5-7 mM (30); that in the heart ranges between 2-3mM (30).
With the exception of the lens of the eye (30), the levels found
in the liver are the highest within the body (11). Noteworthy
is the fact that red blood cells contain four times more GSH
than the plasma (2.0mM vs. .5 mM) (30).
is regulated primarily through excretion. Selenium is excreted
via two main paths: urinary (50-67%) and fecal (40-50%) (13).
Extremely high intakes of selenium can lead to ventilatory elimination
of the mineral in the form of dimethylselenide. Excretion via
the lungs is characterized by a garlic smell odor to the volatile
selenium compound (5,13). Fecal excretion does not appear to
be a major pathway in regulation. Instead, urinary excretion
is the primary route of regulation under normal physiological
conditions. Common to all of the excretory pathways is the lack
of knowledge regarding metabolite formation (5,13).
different selenium-containing proteins (selenoproteins) are known
to be present in animals. Most of these proteins have enzymatic
functions that have been characterized. However, the biochemical
functions of most have yet to be determined. Some hypothesized
functions include: maintenance of the cytochrome P450 system,
DNA repair, enzyme activation, and immune system function. Three
other roles for the element are better understood and described
below. Selenium is best known for the role it plays in the glutathione
peroxidase (GSH-Px) enzyme system. Four separate glutathione
peroxidases have been identified. Within the cell total (GSH-Px)
is distributed ~2:1 between the cytosol and the mitochondrial
matrix (19). The distribution of the enzyme allows for increased
efficiency of free radicals by the GSH-Px system. These enzyme
systems are well established as being the major antioxidant defense
systems within the body. Reduced glutathione is the first line
of defense against free radicals. The glutathione system is key
in the coordination of the water and lipid soluble antioxidant
defense systems (2). The peroxidases use reduced glutathione
to stop peroxidation of cells by breaking down hydrogen peroxide
(H2O2) and lipid peroxides (5,13,19). The majority of research
involving the glutathione system has addressed GSH-Px, the enzyme
responsible for the breakdown of hydrogen peroxide to water.
Adequate levels of the intracellular substrate, reduced glutathione,
are required in order for GSH-Px to exhibit antioxidant properties
(19). As reduced glutathione is utilized to remove H2O2 from
the body, oxidized glutathione is formed. An equally important
enzyme converts oxidized glutathione back to reduced glutathione
for use by the antioxidant defense systems within the body. The
enzyme that catalyzes this reaction is glutathione reductase.
Iodine metabolism also relies heavily on selenium availability.
More specifically the enzyme involved in the conversion of thyroxine
(T4) back to tri-iodothyronine (T3) appears to be selenium dependent
(10). Both of these enzymes play a very important role during
metabolic activities, which in turn demonstrates the importance
of selenium in the system. A summary written by Powers and Ji
(30) suggests that reduced glutathione may also have the ability
to "recharge" other antioxidants in the body. The authors
have summarized that GSH donates electrons, which in turn helps
restore vitamins C and E to their original electron configuration.
Recommended Daily Allowance (RDA)
The National Research
Council established an estimated safe and adequate daily dietary
intake for selenium in 1980. At that time, the recommendation
was set from 50 to 200 micrograms. This recommendation was based
strictly on extrapolation of animal studies, as very few human
studies had been done (5). Since this time, human balance studies
have been performed along with repletion studies in selenium
deficient regions of China. The balance studies have proven to
be very poor indicators of selenium intake because the human
body adjusts its excretion depending on intake of the element.
Repletion studies found that approximately 40 ug per day of selenium
maximized glutathione peroxidase activity (13). This was very
important, as it led to the establishment of a RDA for the element
in 1989 (3,5,13). After some corrections for body weight and
subject variability, the RDA was set at 70 ug for men and 55
ug for women (24). By the year 2001 the National Academy for
Sciences will have eliminated the RDAs and established Dietary
Reference Intakes for all vitamins and minerals. At present time,
selenium is the only antioxidant included herein without a DRI.
Once established, this web site will reflect the new recommended
level. The current levels are easily obtainable through the consumption
of a mixed diet in all areas of North America. However, these
levels would be very hard to reach for those persons living in
countries with selenium poor soil (5,13).
diets can induce a wide host of responses in humans, some of
which are fatal. The first evidence for this was shown in 1979
when a group of Chinese scientists correlated selenium deficiency
with Keshan disease and Kashin-Beck's disease. Keshan disease
is a cardiomyopathy that leads to cardiogenic shock and in some
cases, congestive heart failure. Those with an acute case suffer
from sudden cardiac insufficiency. In chronic cases, subjects
suffer from heart enlargement with varying degrees of insufficiency.
The heart also undergoes necrosis and is replaced with bone (5,13).
Through an intervention study, the protective effects of selenium
were discovered. The research showed that supplementation with
selenium had protective benefits, but could not reverse heart
failure (5). While Keshan disease mainly affects children and
young women, a second disease, Kashin-Beck's Disease, attacks
during pre-adolescence. Kashin-Beck's disease results in severe
osteoarthritis. The disease is often characterized by degeneration
of the nerves and cartilage cells (chondrocytes) of the body.
Damage to the chondrocytes results in dwarfism and joint deformation
(5). Selenium deficiency is often observed in people on total
parenteral nutrition (TPN). Symptoms of selenium deficiency include
muscle pain, weakness, and loss of pigment in the hair and skin
and the whitening of the nail beds (13). Selenium deficiency
can also occur from interaction with other elements. Lead reacts
with selenium and significantly lowers the tissue concentration
of the mineral. The mechanism behind this is presently unclear,
but it has been speculated that the binding of both elements
to sulfhydryl groups may be involved. Iron and copper also seem
to interact with selenium and inhibit uptake of the element.
When the body experiences decreased levels of methionine, it
compensates by incorporating seleno-methionine into body proteins.
This leads to a concomitant decrease in free available selenium
within the body.
studies have been performed with a wide array of outcomes. Studies
carried out in areas having a high selenium content have failed
to establish any specific symptoms of selenium toxicity. Indices
of high selenium diets appear to be hair and nail loss, along
with lesions of the scalp, skin and nervous system, vomiting,
nausea, and fatigue (13). Despite these symptoms, no changes
were observed in the various biochemical tests performed. Intakes
as high as 724-ug/ day have not resulted in adverse side effects
or indices as mentioned above. One known episode of selenium
poisoning did occur in 1984 in the United States. Thirteen people
who consumed supplements from a health food store complained
of nausea, vomiting, weakness, and hair and nail loss. It was
later determined that the supplement contained 182 times the
selenium content listed on the label. Therefore, the subjects
were consuming from 27 to 2387 mg of selenium (5,13). In accordance
with early Chinese studies, the United States Environmental Protection
Agency (U.S. EPA) established a reference dose (Rfd) for selenium.
The Rfd serves as a toxicological standard that is defined as
"an estimate (with uncertainty spanning perhaps an order
of magnitude) of a daily exposure to the human population (including
sensitive subgroups) that is likely to be without an appreciable
risk of deleterious effects during a lifetime". The EPA
has set the ceiling for selenium at 400 micrograms (ug) (5).
Selenium & Exercise
Effects of Exercise
on Selenium Requirements
The majority of
selenium research has addressed the possible role selenium may
have in preventing heart disease and some cancers. A body of
evidence has been established in regards to exercise and selenium.
Multiple studies agree that the glutathione peroxidase (GSH-Px)
system increases as a chronic exercise training adaptation (8,12,15,18,21-22,28-29).
The enzyme, glutathione peroxidase (GSH-Px), is dependent upon
selenium. Without selenium, GSH-Px relinquishes the ability to
degrade H2O2 (30). Burk and Levander (5) reported in their summary
of selenium that deficiency of the mineral rarely exists in western
populations, but may be more prevalent in areas with selenium
poor soil, such as parts of China. The most likely cause of selenium
deficiency in North Americans could likely be traced back to
a diet lacking adequate fruits and vegetables. Exercise training
does not appear to increase the need for selenium intake. Eleven
"moderately trained" males cycled on three consecutive
days at 65% VO2 max. Each cycling session was 90 minutes in duration.
During each exercise session, reduced glutathione levels fell
approximately 55% in the first 15 minutes, whereas, oxidized
glutathione levels increased 28% in the same time period. These
results were similar throughout the three day period (35). A
limited number of studies have shown that selenium supplementation
can decrease oxidative stress and improve antioxidant levels
of the mineral. Tessier et al. (32) concluded that, after a ten-week
endurance and supplementation program, plasma and erythrocyte
GSH-Px activity was significantly increased when compared with
a control group who only trained. Interestingly, glutathione
reductase activity was reduced in both groups of subjects. Two
separate studies utilized sedentary men (25) and both men and
women (12). In both studies, the training protocol consisted
of a running regimen. Ohno et al. (25) implemented a ten-week
training program of 30 km (18 miles) per week, whereas, Evelo
et al. (12) utilized a training program that trained the participants
for a half-marathon (13.1 miles) at the end. The studies were
published four years apart, but both found that erythrocyte glutathione
reductase activity was increased after the training regimens.
Endurance and high intensity training both correlate highly with
increased cytosolic and mitochondrial reduced glutathione and
GSH-Px activities. Adaptation of the enzyme is limited to only
Type I and Type IIa muscles. A known adaptation to endurance
training is an increase in oxidative enzyme activity, which increases
to a greater percent than the reduced glutathione antioxidant
defense system does. The mechanism for these increases has yet
to be understood. A seven-week training regimen involving intermittent
cycle sprint training was used to determine changes in glutathione
reductase and GSH-Px activity. After six weeks, no differences
in enzyme activity were noted. However, muscle biopsies taken
3, 24, and 72 hours after one additional week (week 7) of more
frequent training resulted in significant increases in both enzymes
and markers of anaerobic capacity (15). Tiddus et al. (34) performed
an eight-week study with 13 sedentary human subjects divided
into two groups (7 male, 6 female). After the eight-week training
period, working for 30 minutes at a workload equivalent to seventy
percent of VO2 max (followed by 0-5 minutes of work at 100% VO2
max), both groups had a significantly higher VO2 max. However,
antioxidant status in the pre and post training measurements
was not significantly different. The scientists acknowledged
that their findings were contradictory to some studies. They
attributed these findings to their protocol, which may have not
been intense enough to induce changes in free radical production
and hence the antioxidant defense system (34). However, the protocol
used, closely resembles the training intensity of a large majority
of recreational exercisers. The degree of adaptation may be limited
in humans, also as the body has been shown to have internal excretion
mechanisms that control the amount of endogenous selenium. It
should be noted that, the lack of positive adaptations has also
been exhibited using the laboratory rat. Some will argue that
the results found in the rat may be difficult to extrapolate
to humans. However, rat studies permit more invasiveness than
those of humans. Criswell et al. (8) measured the activity of
GSH-Px in gastrocnemius and soleus muscles. Two exercise protocols
were used. The first involved endurance training while the second
involved use of interval training. The results along with those
from an exercise and aging study (21) found that GSH-Px activity
was significantly increased in the soleus muscle of interval-trained
rats (8). Similar results have also been found in the costal
diaphragm of rats (29). Leeuwenburgh and colleagues (22) have
shown evidence that contradicts those previously mentioned for
the soleus. GSH-Px activity of the soleus did not change in animals
on a ten-week training program. Furthermore, glutathione reductase
activity in the soleus decreased (22). These results are in stark
contrast to the results published by the same group of researchers
three years earlier. However, it should be noted that the sex,
age, and type of rat used in the confounding studies were different.
Powers et al. (28) used the rat model exercising at 30, 60, or
90 minutes at either low (65% VO2 max), medium (75% VO2 max),
or high (85%VO2 max) exercise intensities to investigate antioxidant
enzyme activity. Activity of red gastrocnemius, white gastrocnemius,
and soleus were determined. GSH-Px activity was elevated in the
red gastrocnemius muscle only and was directly related to the
duration of the exercise, but not its intensity. The conflicting
results of the studies provide further evidence that reduced
glutathione upregulation may vary from individual to individual.
These discrepancies could be linked to training protocols, experiment
design, age, sex, or genetic factors.
of Oxidative Stress / Lipid Peroxidation
A strong body
of evidence suggests that free radical production does increase
during times of elevated oxygen intakes, such as those levels
that accompany exercise (1,9,11,16,31). An indirect, but significant
function of selenium is to protect the cell from the oxidative
stress and free radical formation that occurs during exercise.
Selenium can be considered the "rate-limiting" substrate
in the GSH-Px system. Without selenium, the peroxidase enzyme
cannot be formed and consequently, antioxidant protection by
the GSH-Px system is compromised. Multiple studies (21,25) have
shown that, glutathione reductase levels are elevated in both
skeletal muscle and erythrocytes after exposure to chronic exercise.
Reduced nicotinamide adenine dinucleotide phosphate (NADPH),
along with glutathione reductase as a catalyst, converts oxidized
glutathione back to the reduced form. As free radical peroxidation
increases the ratio of reduced glutathione, oxidized glutathione
decreases, hence the ratio is often used as a marker of radical
formation within the body (19). The endogenous increase in the
reduced glutathione antioxidant defense system with chronic training
likely acts as a protective mechanism to help prevent oxidative
stress within the body. Furthermore, it has been established
that both free radical production and GSH-Px activity increase
with exercise. Ortenblad et al. (26) performed a study using
a short-term maximal exercise protocol. Briefly, free radical
muscle damage was evaluated after a continuous 30-second maximum
jump test in both trained and untrained subjects. The resting
muscle levels of glutathione reductase were significantly higher
in the trained (elite volleyball players) versus untrained groups.
Creatine kinase, an indicator of muscle damage, was significantly
higher in the untrained group after exercise. The research supported
the notion that the reduced glutathione defense system is upregulated
and better able to protect muscle from lipid peroxidation in
trained individuals (23). Thus, a likely hypothesis is that,
the endogenous upregulation of the GSH system via chronic exercise
is an adaptive mechanism established to counter-act free radical
in Exercise Recovery
The role selenium
plays in exercise recovery has yet to be established. As for
other roles, it would be as a part of the glutathione system.
Glutatione reductase works to remove H2O2 from the body. One
can conclude that as long as excess hydrogen peroxide and singlet
oxygen is present, the glutatione system will work to remove
the radicals. As part of the initial repair of muscle damage,
an acute inflammatory process takes place. The immune system,
specifically neutrophils, uses free radicals to "mark"
bad or damaged tissue for removal from the body. Instances of
severe muscle damage (i.e. unaccustomed exercise) cause infiltration
of neutrophils and macrophages into the tissue. Neutrophils and
macrophages have a tendency to overkill in order to get all of
the bad tissue. In turn, this means that some healthy tissue
is likely to be damaged in the process (33). Earlier research
(33) has shown that, in damaged muscle, immune system responses
peak between days two and seven. Thus, studies showing the relationship
between the delayed onset of muscle damage and response of the
antioxidant defense system need to be conducted. Superoxide production
can be controlled by antioxidants, such as the glutathione system.
Control of post-exercise free radical production could actually
end up being a counter-productive measure. By removing free radicals
that neutrophils have established to mark tissue, the body is
in fact delaying the exercise recovery process (33). Removal
of the oxidative markers decreases the amount of damaged tissue
that is targeted by the immune system. Endogenous regulation
of the reduced glutathione system could play a role in maintaining
the fine balance of oxidative by-products to antioxidants. Thus,
selenium may play an indirect, but significant role in exercise
recovery. Research addressing this possibility does not exist.
Therefore, the hypothesis presented could be a key in understanding
the possible inhibitory effects of selenium on muscle damage
and antioxidant function.
Summary and Current Recommendations
peroxidase enzyme system is very important in controlling free
radicals in vivo. This particular antioxidant system has no performance-enhancing
benefits. The system is upregulated with exercise, which allows
for better control of the free radicals and lipid peroxidation
increases that occur during unaccustomed or strenuous exercise.
The role GSH-Px plays in exercise recovery has yet to be established.
The author of this literature review has formed a hypothesis
that could be used to explore the topic further. The GSH-Px system
has been shown to have the ability to up-regulate itself via
endurance and/or high intensity training. Furthermore, selenium
soil content is adequate in North America and most of the world.
Those places with low selenium add the mineral to livestock feed.
The adequacy of selenium warrants no need for supplementation
with the mineral. Athletes will gain no competitive advantage
by utilizing selenium as an ergogenic aid or exercise recovery
aid. The toxic effects of the mineral are devastating and can
be detrimental. Therefore, supplementation with the mineral is
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