Research on the Mineral Selenium
The following research abstracts
are presented to reflect the findings of possible benefits from
minerals as a dietary supplement and nutritional supplement.
You will find more on the ionic
selenium page.
Nutrition Research (USA), 1996,
16/3 (505-516)
Combined (internal plus external)
radiation exposure of the population and emergency workers,
as a result of the Chernobyl accident, increased the oncogenic
risk, and to reduce it is a problem of the utmost importance.
A long-term experiment in 400 rats exposed to radiation following
the Chernobyl pattern showed that a selenium-enriched
diet started after exposure caused a longer average lifespan
and a 1.5 - 3.5 fold decrease of leukaemias and other malignancies,
e.g. breast, thyroid and lung cancers, etc., at late times.
Selenium was first demonstrated to provide protection against
late effects which is equivalent to a whole-body dose reduction
by 1.4 Sv (140 rem). The dietary levels of selenium
used were above those accepted as physiological but considerably
below toxic ones (10, 30 and 100 microg Se/day per capita).

Biochemical Pharmacology (USA),
1997, 53/7 (921-926)
The effects of two types of selenium
compounds on the expression levels of growth arrest and DNA
damage-inducible (gadd) genes and on selected cell death genes
were examined in mouse mammary MOD cells to test the hypothesis
that the diversity of selenium-induced
cellular responses to these compounds could be distinguished
by unique gene expression patterns. Whereas the expression patterns
of known cell death-related genes (bcl-2 and bax) were not informative
with respect to the cellular response patterns upon exposure
to selenium compounds, time-dependent
and selenium species-specific induction
patterns were observed for gadd34, gadd45 and gadd153 genes.
It was also observed that the MOD cells expressed a truncated
p53 transcript but no detectable immunoreactive P53 protein,
indicating a null p53 phenotype. The fact that selenium
compounds induced growth arrest and death of these cells and
that these compounds induced specific patterns of expression
of gadd genes indicates that these genes may mediate some selenium-induced
cellular responses. The findings further imply that selenium
compounds may be effective chemopreventive agents for human
breast carcinogenesis, in which p53 mutations are frequent.

Japanese Journal of Thoracic
Diseases (Japan), 1996, 34/12 (1406-1410)
We encountered three patients
with chronic respiratory failure who had heart failure of cardiac
arrhythmias and low levels of serum selenium.
All three had tracheostomies and had received long-term parenteral
nutrition that had not included selenium.
All three also had refractory cardiac dysfunction, which was
manifested in edema, heart failure, and various tachycardias.
We suspected that selenium deficiency
had caused their cardiac dysfunction. Serum selenium
concentrations were found to be much lower than normal in all
three, so 100 microg/day of selenium
was administered in addition to their tube feedings. Cardiac
function improved after replacement of selenium.
These cases show the need for preventing selenium
deficiency in patients with chronic respiratory failure during
long-term administration of parenteral nutrition.

J Am Coll Nutr (UNITED STATES)
Oct 1994, 13 (5) p496-8
OBJECTIVE: The following review
of the literature on the importance of Selenium (Se) in myocardial
homeostasis and of the pharmacology of this trace metal, represents
an attempt to search, without prejudice to other possible explanations,
for a rationale of a beneficial effect of Se substitution as
an adjuvant to antiarrhythmic therapy. background: For several
years, in the early 1980s, I had to deal with the problem of
a serious ventricular arrhythmia (non-sustained and sustained
ventricular tachycardia) which was remarkably resistant to a
battery of the most potent antiarrhythmic agents. Eventually,
dramatic improvement, lasting for a period of 8 years, was achieved
with Flecainide, which, however, left unsolved the episodic
occurrence of disabling ventricular bigemini. Over the most
recent period of 1 year and 8 months, there was a sudden and
unexplained return to unbroken normal sinus rhythm. Among the
multiplicity of possible reasons for this fortunate development,
the concurrent introduction of Se substitution appeared as the
most obvious, though very tentative explanation. Substitution
of this trace metal preceded the extinction of ventricular bigemini
by 1 week and actually represented the sole modification of
otherwise reasonably standardized conditions of antiarrhythmic
therapy, life style and diet. (25 Refs.)

Med Hypotheses (ENGLAND) Oct
1981, 7 (10) p1287-1302
The preventive merits of "nutritional
insurance" supplementation can be considerably broadened
if meaningful doses of nutrients such as mitochondrial "metavitamins"
(coenzyme Q, lipoic acid, carnitine), lipotropes, and key essential
fatty acids, are included in insurance supplements. From the
standpoint of cardiovascular protection, these nutrients, as
well as magnesium, selenium, and
GTF-chromium, appear to have particular value. Sophisticated
insurance supplementation would likely have a favorable impact
on many parameters which govern cardiovascular risk--serum lipid
profiles, blood pressure, platelet stability, glucose tolerance,
bioenergetics, action potential regulation--and as a life-long
preventive health strategy might confer substantial benefit.
(111 Refs.)

Cardiovascular Drugs and Therapy
(USA), 1996, 10/5 (567-571)
Oxidation of low density lipoprotein
is involved in the pathogenesis of atherosclerosis. Epidemiological
studies suggest a negative correlation between the occurrence
of cardiovascular diseases and blood concentrations of lipophilic
antioxidants such as vitamins A and E and beta-carotene. Trace
elements, such enzymes as glutathione peroxidase and superoxide
dismutase. The aim of this study was to determine the antioxidant
and trace element status of patients with severe hypercholesterolemia
who had been treated with dextran-sulphate low-density lipoprotein
apheresis in comparison with two control populations, normocholesterolemic
subjects and untreated hypercholesterolemic patients. Our results
showed that, patients treated with LDL apheresis, compared with
normocholesteromic subjects, were not deficient in vitamin E,
beta-carotene, and copper, but had low plasma levels of selenium,
zinc, and vitamin A. The low selenium
and vitamin A levels were due to the LDL apheresis treatment,
and the hypercholesterolemia might have provoked the low plasma
levels of zinc.This study pointed out the potential benefits
of supplemental selenium, zinc,
and vitamin A in patients being treated with LDL apheresis.

Australian and New Zealand Journal
of Ophthalmology (Australia), 1995, 23/1
Evidence is accumulating that
most of the degenerative diseases that afflict humanity have
their origin in deleterious free radical reactions. These diseases
include atherosclerosis, cancer, inflammatory joint disease,
asthma, diabetes, senile dementia and degenerative eye disease.
The process of biological aging might also have a free radical
basis. Most free radical damage to cells involves oxygen free
radicals or, more generally, activated oxygen species (AOS)
which include non-radical species such as singlet oxygen and
hydrogen peroxide as well as free radicals. The AOS can damage
genetic material, cause lipid peroxidation in cell membranes,
and inactivate membrane-bound enzymes. Humans are well endowed
with antioxidant defences against AOS; these antioxidants, or
free radical scavengers, include ascorbic acid (vitamin C),
alpha-tocopherol (vitamin E), beta-carotene, coenzyme Q10, enzymes
such as catalase and superoxide dismutase, and trace elements
including selenium and zinc. The
eye is an organ with intense AOS activity, and it requires high
levels of antioxidants to protect its unsaturated fatty acids.
The human species is not genetically adapted to survive past
middle age, and it appears that antioxidant supplementation
of our diet is needed to ensure a more healthy elderly population.

AKTUEL. ERNAHR.MED. KLIN. PRAX.
(Germany), 1994, 19/3 (155-159)
The role of antioxidative vitamins
in the therapy of diabetes mellitus is of growing importance.
The development of diabetic late complications (cataract, retinopathy,
nephropathy and neuropathy and others) is associated with an
increased presence of free radicals, and therefore, elevated
oxidative stress of the human body. The aim of the present study
was the evaluation of the vitamin and selenium
status of diabetics. Thirty-eight patients of the age of 35-58
years had been diabetics for 8-27 years and their plasma concentration
of haemoglobin was 6.7-7.5%. The diabetics of type I were treated
with a functional insulin therapy with dietary restrictions,
whereas the type II diabetics received oral antidiabetica (sulfonyl
urea, biguanids) and had to comply with a fixed diet. Any supplementation
of vitamins was omitted. The nutritional intake was monitored
by a weighed record over 7 days. The plasma concentrations of
vitamin A, beta-carotene, K and E were determined by reversed-phase-PLC.
For the assessment of vitamin C concentrations, a photometric
method was used, and selenium concentrations
was determined by electrothermal atomic absorption spectrometry.
Mean values of plasma concentrations were: vitamin A 36-50 microg/dl,
beta-carotene 35-42 microg/dl, vitamin K: 0.5-0.6 ng/ml, vitamin
E: 1.1-1.6 mg/dl, selenium: 72-75
microg/l. The values of vitamin C concentration of the diabetics
type I without late complications and of type II diabetics were
at 0.8 mg/dl and, therefore, at the borderline. Diabetics of
type I with late complications showed marginal values of 0.6
plus or minus 0.3 mg/dl. The critical value for the prevention
of scorbut has been fixed at 0.4 mg/dl. The results of this
confirm the importance and efficiency of vitamins, especially
of ascorbic acid. Positive effects of this antioxidative vitamin
in respect of the prevention of diabetic side effects and subsequent
disease should therefore be expected.

Stedman J.D.; Spyrou N.M.; Millar
A.D.; Altaf W.J.; Akanle O.A.; Rampton D.S.
J.D. Stedman, Department of Physics, University of Surrey, Guildford,
Surrey GU2-5XH United Kingdom
Journal of Radioanalytical and Nuclear Chemistry (Hungary) ,
1997, 217/2 (189-191)
Ulcerative colitis (UC) is a
type of inflammatory bowel disease (IBD) in which there is recurrent
inflammation of the mucous membranes of the colon. Inflammation
is accompanied by the production of reactive oxygen species
(ROS) including, amongst others, hydrogen peroxide. Selenium
in the form of the selenoprotein glutathione peroxidase (GSH-Px)
acts as a catalyst in the reaction which reduces hydrogen peroxide
to watch. It may therefore beneficial to supplement the diets
of patients who suffer from UC with selenium.
In this preliminary study nine patients suffering from moderate
UC were supplemented with selenium-beta
tablets (300 microg Se per tablet) twice daily. Blood samples
were taken at the start of the trial and at 1, 2 and 4 week
intervals. Freeze-dried serum samples were analysed for their
selenium content using the technique
of instrumental neutron activation analysis (INAA). Samples
were also analysed by particle induced X-ray emission (PIXE)
to monitor other trace elements levels. Selenium concentrations
were found to increase during supplementation and iron concentrations
to decrease. Stool frequency was also found to improve suggesting
that ROS may be important in the pathogenesis of UC.

Cancer Res. 1994 Apr 1. 54(7
Suppl). P 2029s-2031s
In Linxian China, the esophageal/gastric
cardia cancer mortality rates are among the highest in the world.
There is suspicion that the population's chronic deficiencies
of multiple micronutrients are etiologically involved. We conducted
two randomized, placebo-controlled nutrition intervention trials
to test the effects of vitamin and mineral supplements in lowering
the rates of esophageal/gastric cancer. In the first trial,
the dysplasia trial, 3318 adults with a cytological diagnosis
of esophageal dysplasia received daily supplementation with
26 vitamins and minerals in doses typically 2-3 times the United
States Recommended Daily Allowances, or placebos, for 6 years.
The second trial, the general population trial, involved 29,584
adults and used a one-half replicate of a 2(4) factorial experimental
design which tested the effects of four combinations of nutrients:
A, retinol and zinc; B, riboflavin and niacin; C, vitamin C
and molybdenum; and D, beta-carotene, vitamin E, and selenium.
Doses for these daily supplements ranged from 1 to 2 times the
United States Recommended Daily Allowances, and the different
vitamin/mineral combinations or placebos were taken for a period
of 5.25 years. As part of the general population trial, and
end-of-intervention endoscopy survey was carried out in a small
(1.3%) sample of subjects to see if supplementation affected
the prevalence of dysplasia and early cancer. Herein we review
the methods of these trials and the results of the endoscopic
survey. Fifteen esophageal and 16 gastric cancers were identified
in endoscopic biopsies from the 391 subjects evaluated from
two villages, and nearly all were asymptomatic. No significant
reductions in the prevalence of esophageal or gastric dysplasia
or cancer were seen with any of the four supplement groups.
However, the prevalence of gastric cancer among participants
receiving retinol and zinc was 62% lower than those not receiving
those supplements (P = 0.09), while participants receiving beta-carotene,
vitamin E, and selenium had a 42%
reduction in esophageal cancer prevalence (0.34). We have reported
separately that cancer mortality over the entire 5.25-year period
was significantly reduced among those receiving beta-carotene,
vitamin E, and selenium. The findings
from the overall trial and the endoscopic sample offer a hopeful
sign and should encourage additional studies with these agents
in larger numbers of subjects.
