Selenium is a
non-metal 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 places 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) have
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 too 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-iodothryronine (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
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 the 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
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
whom 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) report 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 on 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, convert 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
benefit. 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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