Agriculture Reference
In-Depth Information
effects are rare, in one study these may have accounted for increased mortality in the
supplemented group (Doherty et al. 1998). More is not necessarily better.
selenIum
Selenium was a little-known trace element in human health until recently, when two
questions came under scrutiny: the role of oxidative stress in disease and the cause
of Keshan disease.
Selenium is essential for the pivotal antioxidant glutathione peroxidase. This
enzyme helps protect cells from the damaging effects of oxidation, for example, by
ultraviolet radiation of skin, by exogenous toxins in the liver, or from any excess of
“normal” oxidative processes that are used, for example, to damage and kill invading
bacteria. Glutathione peroxidase acts on lipid peroxides and hydrogen peroxide to
produce harmless hydroxy acids and water, respectively (Geissler and Powers 2006).
In the 1980s, the “free-radical” theory of the etiology of edematous malnutrition
was supported by evidence of deficiencies in several antioxidant systems, including
glutathione peroxidase (Golden and Ramdath 1987). Since then, evidence has accu-
mulated for a role of oxidative stress in several other common, chronic diseases, such
as atherosclerosis and arthritis.
Keshan disease was described to the Western world also in the 1980s. It is charac-
terized by a cardiomyopathy present in thousands of youngish women and children
living in a specific region in southwest China in which soil selenium is particu-
larly low. In large studies, selenium supplements appeared to prevent, although not
treat, the disease. Later, it was observed that there were temporal fluctuations in
Keshan disease (Geissler and Powers 2006). Enteroviruses were implicated, espe-
cially Coxsackie virus B4. This led to mouse experiments in which it was shown
that increased oxidative stress, induced by deficiency of either selenium or vitamin
E in mice infected with nonvirulent Coxsackie virus (B3/0), could induce mutations
in the virus, causing it to become virulent (Beck et al. 2003). Indeed, high intakes of
polyunsaturated fatty acids (PUFAs) or iron had similar effects, also explained by
increased oxidative stress. Thus, it appears that Keshan disease is not a direct effect
of selenium deficiency; rather, it is due to the effect of oxidative stress on infecting
viruses. This shows how complex interactions are, not only between micronutrients
themselves, but also between micronutrients and human metabolism and even the
metabolism of invading microorganisms.
Another pair of interesting selenoenzymes are thyrodoxin and iodothyronine
deiodinase. Both are involved in thyroid metabolism, which of course is also highly
dependent on iodine supply.
1
Selenium deficiency exacerbates the effects of iodine
deficiency (Geissler and Powers 2006). In the face of both deficiencies, giving iodine
without selenium does not adequately treat the features of iodine deficiency disor-
ders (IDD). This was also observed in south China, where the iodine-deficient belt
overlaps the selenium-deficient belt.
Another important role of selenium, also related to its antioxidant function, is in
prevention of a variety of malignancies, including the increasingly common pros-
tate cancer.
