Iron Absorption in
Young Indian Women: The Interaction of Iron Status with the
Influence
of Tea and Ascorbic Acid
Thankachan P, et al.
Am J Clin Nutr 2008 ;87:881-6.
Ascorbic acid (AA) enhances and tea inhibits iron
absorption. It is unclear whether iron status influences the
magnitude of this effect. We evaluated the influence of the
iron status of young women on iron absorption from a rice
meal with or without added tea or AA. Two stable-isotope
iron absorption studies were made in 2 groups of 10 subjects
with iron deficiency anemia (IDA) and 10 subjects who were
iron replete (control subjects). In study I, the reference
rice meal was fed alone or with I or 2 cups of black tea. In
study 2, the reference meal was fed alone or with AA (molar
ratio to iron, 2: I or 4: I). Iron absorption was measured
by the erythrocyte incorporation of 57Fe and 58Fe labels at
14 d. Mean fractional iron absorption from the reference
rice meal was =2.5 times as great in the IDA group as in the
control group. The consumption of 2 cups of tea decreased
iron absorption in the control subjects by 49% or 66%
respectively, and in the IDA group by 59% or 67%,
respectively. AA (molar ratio to iron, 2:1 or4:1) increased
iron absorption by 270% or 343%, respectively, in control
subjects and by 291% or 350%, respectively, in subjects with
IDA. The inhibitory effect of tea and the enhancing effect
of AA on iron absorption were similar in the 2 groups.
Overall differences in iron absorption in the 2 groups,
however, continued to be dictated by iron status.
Magnesium Deficiency
Accelerates Cellular Senescence in Cultured Human
Fibroblasts
Killilea DW, et al.
Proc Natl Acad Sci USA, 2008 Apr 15 ;105(15) :5768-73.
Magnesium inadequacy affects more than half of the U.S.
population and is associated with increased risk for many
age-related diseases, yet the underlying mechanisms are
unknown. Altered cellular physiology has been demonstrated
after acute exposure to severe magnesium deficiency, but few
reports have addressed the consequences of long-term
exposure to moderate magnesium deficiency in human cells.
Therefore, IMR-90 human fibroblasts were continuously
cultured in magnesium-deficient conditions to determine the
long-term effects on the cells. These fibroblasts did not
demonstrate differences in cellular viability or plating
efficiency but did exhibit a decreased replicative lifespan
in populations cultured in magnesium-deficient compared with
standard media conditions, both at ambient (20% 0(2)) and
physiological (5% 0(2)) oxygen tension. The growth rates for
immortalized
IMR-90 fibroblasts were not affected under the same
conditions. IMR-90 fibroblast populations cultured in
magnesium-deficient conditions had increased
senescence-associated beta-galactosidase activity and
increased p16(INK4a) and p21(WAF1) protein expression
compared with cultures from standard media conditions.
Telomere attrition was also accelerated in cell populations
from magnesium-deficient cultures. Thus, the long-term
consequence of inadequate magnesium availability in human
fibroblast cultures was accelerated cellular senescence,
which may be a mechanism through which chronic magnesium
inadequacy could promote or exacerbate age-related disease.
Selenium Inhibits High Glucose- and High
Insulin-induced Adhesion Molecule Expression in Vascular
Endothelial Cells
Zheng HT, et al.
Arch Med Res, 2008 ;39(4) :373-9.
Initiation of an atherosclerotic lesion requires endothelial
expression of adhesion molecules. Selenium (Se), a
biologically essential trace element, can inhibit cytokine
(e.g., TNF-alpha)-induced expression of adhesion molecules.
Atherosclerosis is accelerated in diabetic patients. This is
at least partially caused by hyperglycemia and
hyperinsulinemia increasing adhesion molecule expression.
These experiments tested whether Se can also alter high
glucose- and high insulin-induced expression of adhesion
molecules. Human umbilical vein endothelial cells (HUVECs)
were pretreated with Se and stimulated by high glucose or
high insulin. Expression of adhesion molecules was measured
by Western blot. Se (100 mmol/L) significantly inhibited
glucose (25 mmol/L)- induced expression of vascular cell
adhesion molecule-1 (VCAM-1), intercellular adhesion
molecule-1 (ICAM-1), and E-selectin.
Moreover, Se significantly inhibited insulin (100 mmol/L)-induced
VCAM-1 and ICAM-1 expression, whereas high insulin had no
inducing effect on E-selectin. Se also inhibited high
glucose- and high insulin-induced activation of p38
mitogenactivated protein kinase (p38), which indicated that
the preventive effects of Se on adhesion molecules may be
associated with p38. The important role of p38 in Se effects
was further confirmed using p38 inhibitor SB203580. These
results suggest that Se can inhibit high glucose- and high
insulin-induced expression of adhesion molecules. Such
antagonism is at least partially mediated through the
modulation of p38 pathway. Therefore, Se may be considered
as a potential preventive intervention for
diabetes-accelerated atherosclerosis.
Plasma Selenium Measurements in Subjects
from Areas with Contrasting Gastric Cancer Risks in Columbia
Camargo MC, et al.
Arch Med Res, 2008 ;39(4) :443-51.
An inverse association between selenium status and
incidence of different neoplasias including gastric cancer
has been reported. This pilot study aimed to determine and
compare selenium status in two Colombian populations with
different gastric cancer risks: a high-risk area in the
volcanic region of the Andes Mountains and a low-risk area
on the Pacific coast. Eighty nine adult males were recruited
in the outpatient clinics of two public hospitals (44 and 45
from high- and low-risk areas, respectively) and provided a
blood sample. Seventy one (79.8%) participants underwent
upper gastrointestinal endoscopy. Plasma selenium was
assayed using a fluorometric method, selenoprotein-P by
ELISA, and glutathione peroxidase activity by a
spectrophometric method. Histological diagnosis and
Helicobacter pylori infection were evaluated in gastric
biopsy samples. Unpaired samples t-test and linear
regression analyses were used for statistical analyses.
Although none of the subjects in either of the two
geographic areas was selenium deficient, the level of plasma
selenium was significantly lower in men from the high-risk
area compared with those
from the low-risk area. Levels of selenoprotein-P and
glutathione peroxidase activity were similar between groups
after
adjustment for confounders. Selenium measurements were not
associated with histopathological diagnosis. The high
incidence of gastric cancer in the Andean region of Colombia
is unlikely to be explained by selenium deficiency. We
cannot exclude, however, that suboptimal selenium levels may
exist in the gastric mucosa of subjects in the high-risk
area. Therefore, the benefit of selenium supplementation in
gastric cancer prevention cannot be dismissed.
Combination of Selenium and Three Naturally Occurring
Antioxidants Administration
Protects d: -Galactosamine-induced Liver Injury in Rats
Catal T, Bolkent S .
Biol Trace Elem Res, 2008 ;122(2) :127-36.
D: -Galactosamine (D: -GaIN) is a highly selective
hepatotoxin that causes liver injury similar to human
viral hepatitis via depletion of uridine nucleotides,
which subsequently diminishes synthesis of RNA and
proteins. The aim of this study was to investigate the
role of selenium, ascorbic acid, beta-carotene, and
alpha-tocopherol on D: -GaIN -induced liver injury of
rats by morphological and immunohistochemical means. In
this study, Sprague-Dawley female rats were divided into
four groups. Group I consists of rats injected
physiologic saline solution intraperitoneally. Group II
consists of rats given selenium (0.2 mg/kg per day),
ascorbic acid (100 mg/kg per day), beta-carotene (15
mg/kg per day), and alphatocopherol (100 mg/kg per day)
for 3 days via gavage method. Group III consists of the
single dose of D: -GaIN (500 mg/kg)-injected animals.
Group IV are the D: -GaIN - injected animals given the
same antioxidant combination. In situ terminal
deoxynucleotidyl transferase-mediated 2'-deoxyuridine
5'-triphosphate nick-end labeling (TUNEL) assay was
applied to determine apoptosis for paraffin sections of
the liver samples. Moreover, caspase-3 and proliferating
cell nuclear antigen antibody were applied for paraffin
sections. In the group given D: -GaIN, apoptotic cells
with TUNEL assays and caspase-3 activity, which are
liver injury markers induced by D: -GaIN, the hepatocyte
proliferation with cell proliferation assay increased.
However, selenium and other three antioxidants
combination clearly suppressed an increase in apoptotic
cells with TUNEL assay and caspase-3 activity. In
addition, it suppressed D: -GaiNinduced cell
proliferation in the liver. As a result, these results
indicate that selenium and three naturally occurring
antioxidants shows a protective effect against liver
injury induced by D: -GaIN. These results suggest that
supplementation with the combination of selenium,
ascorbic acid, beta-carotene, and alpha-tocopherol may
help prevent the development of liver injury.
Zinc Deficiency and Clinical
Practice—Validity of Zinc Preparations.
Yanagisawa H.
Yakugaku Zasshi, 2008 ;128(3) :333-9.
Zinc is an essential trace element and serves as the
active center of approximately 300 enzymes. Therefore,
zinc deficiency may be associated with a variety of
clinical features such as hypogeusia, hyposmia, growth
retardation, dermatitis, alopecia, gonadal hypofunction,
abnormal pregnancy, susceptibility to infections,
delayed wound healing, impaired glucose tolerance, and
increased carcinogenesis. Zinc deficiency was reported
to be on the increase in the Nagano Study conducted from
2003 to 2005. Zinc therapy is classified into two
categories, zinc-supplementary and specific treatments.
Ordinarily, zinc-supplementary therapy is carried out
for the symptoms and diseases caused by zinc deficiency.
On the other hand, zinc-specific therapy is applied to
obtain copper- and iron-chelating, antifibrotic, and
antidiabetic effects. The availability of zinc-specific
therapy is now confirmed in humans and animals.
Hereafter, the safety of zinc therapy needs to be
examined further.
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