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Introduction
Selenium is only required in the system in microgram
amounts. Selenium is involved in the production of antibodies
and in the elimination of unwanted micro organisms and
thus plays a role in disease resistance.
Role of selenium
- Lescure et al (2000) identified
5 selenoproteins based on RNA structural tags
- Selenoprotein P – contributes
to selenium transportation, has a redox function and
may protect cell membranes (Burke & Hill, 2000)
- Thiroredoxin reductase (contains
selenium) is important for synthesis of deoxy nucleotides
and maintaining redox status of the cell (Lescure
et al, 2000)
- Selenoproteins 15 Kd and 34 Kd
function are unknown but both proteins have a preference
for testicular and prostate tissues (Behne et al,
2000)
- Selenoprotein W function is unknown,
declines from tissues except the brain
Function
of selenium in reproduction
With regard to research work the following
has been ascertained:
- Cattle fed selenium supplementation
is beneficial to maintaining sperm mobility in vitro.
Percent mobility expressed as total mobile sperm per
total sperm counted increased significantly (Phosphorous
less than .05%) as concentration of selenium increased
from 0 to 1.0 ppm (Julien and Murray, 1977)
Interactions of glutathione peroxidase
(GSH-PX), vitamin E, and sulphur-containing amino acids
– The following is a discussion taken from Rotruck
et al. (1973) and Smith et al. (1974): The metabolic
role of selenium in animals seems to be linked with
Vitamin E and sulphur amino acids. Selenium has a sparing
effect on Vitamin E and delays the onset of deficiency
syndromes. Likewise, Vitamin E and sulphur amino acids
partially protect against or delay the onset of several
forms of selenium deficiency syndromes.
Several groups of investigators have emphasized the
role of GSH peroxidase as the primary mechanism for
degrading low levels of H20 in cells. Since GSH peroxidase
also acts on hyproperoxides of unsaturated fatty acids,
the enzyme plays an important role in protecting membrane
lipids, and thus the cell membranes, from oxidative
disintegration. Failure of peroxide destruction can
explain the hemolysis in vitro and oxidative damage
to hemoglobin and possibly the wide variety of degenerative
conditions that occur in selenium deficiency.
A role for selenium in GSH peroxidase may also account
for the apparent 'antioxidant' effects of dietary selenium
observed by previous workers.
- Protection against oxidative damage
to susceptible non-membrane proteins by dietary selenium
but not by vitamin E might explain why some nutritional
diseases respond to selenium but not to vitamin E
- On the other hand, certain tissues
or subcellular components may not be adequately protected
from oxidant damage because they are inherently low
in GSH peroxidase, even with adequate dietary selenium
Selenium spares Vitamin
E in the following:
- Required to preserve integrity
of the pancreas, which allows normal fat digestion
and thus normal vitamin E absorption
- Reduces amount of vitamin E required
to maintain integrity of lipid membranes via GP
- Aids in some unknown way in the
retention of vitamin E in the blood plasma.
Vitamin E reduces selenium
requirement in the following:
- By maintaining body selenium in
an active form or preventing loss from the system
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