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.
Ponz de Leon M; Roncucci L
Dept. of Internal Medicine, University of Modena, Italy.
Scand J Gastroenterol Suppl (NORWAY) 1997, 222 p72-5
Chemoprevention can be defined
as an attempt at cancer control in which the occurrence of the
disease is prevented by the administration of one (or more)
chemical compounds. Main problems in chemoprevention studies
are the choice of a suitable drug, the choice of an appropriate
intermediate or definitive end point, and the definition of
the population which should be investigated. Main classes of
chemopreventive agents include vitamins, non-steroid anti-inflammatory
drugs, minerals such as calcium or selenium,
and other antioxidants such as N-acetylcysteine. Chemoprevention
is particularly appealing in colorectal cancer, either because
these lesions develop through a multistep process, or owing
to the concept of "field carcinogenesis'. Between 1985
and 1990 we carried out a controlled study in which antioxidant
vitamins or lactulose were used in an attempt to prevent the
recurrence of colorectal polyps after their endoscopic removal.
Among the 209 patients who could be evaluated, polyps recurred
in 5.7% of the individuals who were given vitamins (A, C and
E), 14.7% of patients given lactulose and 35.9% of untreated
controls (chi 2 = 17.1, P <0.001). The study suggested that
either antioxidant vitamins or lactulose could be effective
in reducing the recurrence rate of adenomatous polyps. In a
subsequent on-going study, lower doses of the same vitamins
were tested versus N-acetylcysteine (60a 40% reduction of the
recurrence of polyps versus controls) in individuals given N-acetylcysteine,
while the effect of lower doses of vitamins was less appreciable.
Definitive results of the study should be available by the end
of 1998.
Mukherjee B; Sarkar A; Chatterjee
M
Department of Pharmaceutical Technology, Jadavpur University,
Calcutta, India.
Eur J Cancer Prev (ENGLAND) Dec 1996, 5 (6) p455-63
Supplementation of selenium
in the form of selenomethionine (8 ppm) in drinking water daily
has been found to be highly effective in reducing cancer incidence
in male Sprague-Dawley rats fed 2-acetylaminofluorine (2-AAF)
(0.05%) in the basal diet daily for 16 weeks. Selenomethionine
treatment before initiation, during initiation or during the
selection/promotion phases of hepatocarcinogenesis has been
found to be effective in elevating hepatic microsomal cytochrome
b5, cytochrome P-450 contents, triphosphopyridine nucleotide-cytochrome
c-reductase and cytosolic aryl hydrocarbon hydroxylase activities
to a statistically significant level measured either in the
hyperplastic nodules or in the non-nodular surrounding liver
parenchyma compared with 2-AAF control rats. Moreover, selenomethionine
treatment throughout the study also decreased the cytosolic
1-chloro-2,4-dinitrobenzene conjugated glutathione-S-transferase
and microsomal UDP-glucuronyl transferase activities to a significant
level when compared with 2-AAF control rats. Furthermore, direct
correlations between hyperplastic nodules and non-nodular liver
areas were observed with the hepatic selenium
content and also with the rates and patterns of hepatic drug
metabolism. Selenomethionine was also found to protect and improve
the histopathological indices without any toe haematoxylin and
eosin staining. Our results establish the fact that selenium
is particularly protective in limiting the action of 2-AAF during
the initiation phase of hepatocarcinogenesis.
Badmaev V; Majeed M; Passwater
RA
Sabinsa Corporation, Piscataway, NJ, USA.
Altern Ther Health Med (UNITED STATES) Jul 1996, 2 (4) p59-62,
65-7
Selenium is an essential trace
element in nutrition for the prevention of disease in humans.
Epidemiological studies indicate an association between low
nutritional selenium status and
increased risks of cardiomyopathy, cardiovascular disease, and
carcinogenesis in various sites of the body. The role of selenium
supplementation in the prevention and treatment of AIDS-related
pathology has been considered. Selenoproteins discovered in
mammalian cells may account for the essentiality of selenium
in the body's antioxidant defense; thyroid hormone function;
immune system function, particularly the cellular immunity;
formation of sperm; and functioning of the prostate gland. The
seleno-organic compounds, primarily L-(+)-selenomethionine,
generally are recognized as safe and effective forms of selenium
supplementation. The nutritionally recommended dose of elemental
selenium is estimated at 50 to
200 mg per day. There is, however, increased discussion of a
pharmacological dose of selenium,
significantly higher than the nutritional dose of the microelement,
to treat active conditions. One way of increasing the tissue
levels of selenium is to combine
its ingestible form with a nutrientilability enhancing compound.
(87 Refs.)
Neve J
Universite Libre de Bruxelles, Institut de Pharmacie, Belgium.6277
J Cardiovasc Risk (ENGLAND) Feb 1996, 3 (1) p42-7
Selenium is a powerful antioxidant
regulating the activity of the glutathione peroxidase enzymes,
which catalyse the detoxification of hydrogen peroxide and organic
hydroperoxides. Selenium deficiency has been implicated in the
aetiopathogeny of Keshan disease, an endemic cardiomyopathy
observed in China, and in other cases of congestive cardiomyopathy
in subjects on artificial nutrition. However, the evidence from
case-control and prospective studies for an association between
low selenium status and cardiovascular
diseases remains controversial. Mechanisms whereby selenium
protects against such diseases include increased resistance
of low-density lipoproteins against oxidative modification,
modulation of prostaglandin synthesis and platelet aggregation,
and protection against toxic heavy metals. The therapeutic benefit
of selenium administration in the
prevention and treatment of cardiovascular diseases still remains
insufficiently documented.
Vitoux D; Chappuis P; Arnaud
J; Bost M; Accominotti M; Roussel AM
Laboratoire central de biochimie, hopital Lariboisiere, Paris,
France.
Ann Biol Clin (Paris) (FRANCE) 1996, 54 (5) p181-7
In the last five years, there
has been a renewal of interest in the protective role of selenium
in vascular disorders, inspired by experimental evidence that
this trace element could modulate leukotriene and prostaglandin
synthesis in both endothelial cells and platelets. In people
living in low-selenium areas, a
relationship has been established between a decrease in plasma
selenium and an increase in the
risk of coronary disease, atherosclerosis, platelet hyperaggregability
and synthesis of proaggregant and proinflammatory compounds
like thromboxane A2 and leukotrienes. Selenium, as an essential
part of glutathione peroxidase, takes part in the reduction
of hydrogen peroxides and lipid peroxides. The concentration
of these peroxides, in turn, regulates the activities of cyclooxygenase
and lipooxygenase pathways, ultimately influencing the production
of eicosanoids and modulating the balance between a proaggregatory
and antiaggregatory state. Recent evidence shows that selenium,
via its action on glutathione peroxidase activity, may be primarily
responsible for the regulation of the endogenous hydroperoxide
level. In human platelets, the activity of glutathione peroxidase
is particularly high and is very sensitive to the requirement
of selenium. This sensitivity could
explain why platelets of selenium-deficient
subjects show increased aggregation, thromboxane B2 production
and synthesis of the lipoxygenase-derived compounds. In these
deficient subjects, selenium administration
increases platelet glutathione peroxidase activity and inhibits
platelet hyperaggregation and leukotriene synthesis. These results
support the hypothesis that selenium
supplementation has a positive effect on platelet aggregation
in selenium-deficient subjects.
In France, more than 10% of the population is selenium-deficient
and long-term supplementation with low doses of selenium
could have a beneficial effect on the prevention of both thrombosis
and coronary heart disease in these subjects. (35 Refs.)
Levander OA; Whanger PD
U.S. Department of Agriculture, Agricultural Research Service,
Beltsville Human Nutrition Research Center, MD 20705, USA.
J Nutr (UNITED STATES) Sep 1996, 126 (9 Suppl) p2427S-2434S
Information is presented regarding
the approaches that have been used to establish dietary recommendations
for selenium and iodine. In the
case of selenium, activity of the
selenoenzyme glutathione peroxidase has served as a convenient
biochemical endpoint for judging nutritional status. However,
there are differences of opinion among various nutritionists
as to whether full expression of this enzymatic activity is
required for adequate nutriture, thereby resulting in differences
in dietary recommendations. Endpoints for assessing selenium
overexposure are much less satisfactory, but toxicological standards
for selenium have nevertheless
been established. Thus far, no nutritionists have attempted
to shift the paradigm for determining dietary selenium
recommendations away from prevention of deficiency disease to
prevention of chronic degenerative disease (e.g., cancer). In
the case of iodine, urinary excretion of the element is the
most widely used endpoint for judging nutritional status. Numerous
epidemiological surveys have been conducted to determine the
level of urinary iodine excretion that is consistent with prevention
of goiter, the most common endpoint of iodine deficiency. Because
dietary iodine is essentially quantitatively excreted in the
urine, determination of the latter in goitrous areas will allow
an almost direct estimation of those intakes at risk of developing
deficiency disease. Iodine toxicity is complicated by the fact
that some persons are quite tolerant to the element whereas
others are highly sensitive to it. There are relatively complete
data sets concerning exposure vs. human health effects for both
selenium and iodine so that sounder
bases probably exist for their dietary recommendations than
for many other trace elements.
Selenium is an essential trace
element in nutrition for the prevention of disease in humans.
Epidemiological studies indicate an association between low
nutritional selenium status and
increased risks of cardiomyopathy, cardiovascular disease, and
carcinogenesis in various sites of the body. The role of selenium
supplementation in the prevention and treatment of AIDS-related
pathology has been considered. Selenoproteins discovered in
mammalian cells may account for the essentiality of selenium
in the body's antioxidant defense; thyroid hormone function;
immune system function, particularly the cellular immunity;
formation of sperm; and functioning of the prostate gland. The
seleno-organic compounds, primarily L-(+)-selenomethionine,
generally are recognized as safe and effective forms of selenium
supplementation. The nutritionally recommended dose of elemental
selenium is estimated at 50 to
200 mg per day. There is, however, increased discussion of a
pharmacological dose of selenium,
significantly higher than the nutritional dose of the microelement,
to treat active conditions. One way of increasing the tissue
levels of selenium is to combine
its ingestible form with a nutrient bioavailability enhancing
compound. (87 Refs.)
Arora AS; Gores GJ
Center for Basic Research in Digestive Diseases, Mayo Clinic
and Foundation, Rochester, Minnesota 55905, USA.
Semin Liver Dis (UNITED STATES) Feb 1996, 16 (1) p31-8
No abstract.
Jao SW; Shen KL; Lee W; Ho YS
Division of Colon and Rectal Surgery, National Defense Medical
Center, Tri-Service General Hospital Taipei, Taiwan, Republic
of China.
Dis Colon Rectum (UNITED STATES) Jun 1996, 39 (6) p628-31
PURPOSE: This study was designed
to determine the cancer prevention and therapeutic effects of
selenium on rats treated with 1,2-dimethylhydrazine
(DMH). METHODS: One hundred sixty Spraque-Dawley male rats were
divided into seven groups and received 20 mg/kg/week DMH, subcutaneously
for 20 weeks. Two different dosages of selenium
(8 and 4 ppm) were administered to the rats through drinking
water during DMH treatment (B and C groups) or one month before
and during DMH treatment (D and E groups). The rats of Groups
A (control group), B, C, D, and E were killed immediately after
the last DMH injection. The incidence of intestinal cancer in
each group was compared. Eight ppm selenium
was also administered to rats after DMH treatment (Group F),
and survival times were observed and compared with Group G (treated
with DMH only). RESULTS: Rats of Groups B and D received 8 ppm
selenium and had a significantly
decreased incidence of intestinal cancer (from 65.8 percent
(Group A) to 33.3 percent (Group B) and 27.8 percent (Group
D); P = 0.0225 and 0.0038). Rats receiving 4 ppm selenium
had a relatively decreased incidence of intecent (Group A) to
44.4 percent (Group C) and 47.1 percent (Group E) but P >
0.05). Survival time of Groups F and G showed no difference.
CONCLUSIONS: Eight ppm selenium
provided via drinking water has a significant intestinal cancer
prevention effect in the presence of a high dose of DMH (20
mg/kg x 20 weeks), and the cancer therapeutic effect of selenium
is doubtful in this animal model.
Saito N
Nippon Rinsho (JAPAN) Jan 1996, 54 (1) p59-66
It is known that the peroxidation
of LDL is a trigger for developing arteriosclerosis. The oxidized
LDL is produced by either oxidative stress or a few oxidant.
Selenium decreased in serum and some organs of stroke-prone
spontaneously hypertensive rats (SHRSP), which is a cofactor
of glutamine peroxidase. Serum magnesium decreased in patients
with diabetes mellitus, with ischemic heart disease, with essential
hypertension and with cerebral vascular lesions. Calcium to
magnesium ratio was higher in some organs of SHRSP as compared
to Wistar Kyoto rats (WKY). These changes accelerated vascular
lesions in SHRSP. (21 Refs.)
Crit Rev Food Sci Nutr (UNITED
STATES) Apr 1997, 37 (3) p211-28
Selenium (Se) was discovered
180 years ago. The toxicological properties of Se in livestock
were recognized first; its essential nutritional role for animals
was discovered in the 1950s and for humans in 1973. Only one
reductive metabolic pathway of Se is well characterized in biological
systems, although several naturally occurring inorganic and
organic forms of the element exist. The amount of Se available
for assimilation by the tissues is dependent on the form and
concentration of the element. Se is incorporated into a number
of functionally active selenoproteins, including the enzyme
glutathione peroxidase, which acts as a cellular protector against
free radical oxidative damage and type 1 iodothyronine 5'-deiodinase
which interacts with iodine to prevent abnormal hormone metabolism.
Se deficiency has been linked with numerous diseases, including
endemic cardiomyopathy in Se-deficient regions of China; cancer,
muscular dystrophy, malaria, and cardiovascular disease have
also been implicated, but evidence for the association is often
tenuous. Information on Se levels in foods and dietary intake
is limited, and an average requirement for Se in the U.K. has
no been established. Available data suggest that intake in the
U.K. is adequate for all, except for a few risk groups such
as patients on total parenteral nutrition or restrictive diets.
(122 Refs.)
