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SERUM SELENIUM PREDICTS LEVELS OF
F2-ISOPROSTANES AND PROSTAGLANDIN F2ALPHA IN A 27 YEAR
FOLLOWUP STUDY OF SWEDISH MEN.
Helmersson J, et al.
Free Radic Res, 2005; 39(7):763-70.
Low concentrations of selenium (Se) predict mortality
and cardiovascular diseases in some populations. The effect
of Se on in vivo indicators of oxidative stress and
inflammation, two important features of atherosclerosis, in
human populations is largely unexplored. This study
investigated the longitudinal association between serum
selenium (s-Se) and a golden standard indicator of oxidative
stress in vivo (8-iso-prostaglandin F2alpha, a major
F2-isoprostane), an indicator of cyclooxygenase
(COX)-mediated inflammation (prostaglandin F2alpha), high
sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6)
and serum amyloid A protein (SAA) in a follow-up study of 27
years. The s-Se was measured in 615 Swedish men at 50 years
of age in a health investigation. The status of oxidative
stress and inflammation was evaluated in an investigation 27
years later by quantification of urinary 8-iso-PGF2alpha and
15- keto-dihydro-PGF2alpha (a major metabolite of PGF2alpha)
and serum hsCRP, SAA and IL-6. Men in the highest quartile
of s-Se at age 50 had decreased levels of 8-iso-PGF2alpha
compared to all lower quartiles and decreased levels of
PGF2alpha compared to all lower quartiles at follow-up.
These associations were independent of BMI, diabetes,
hyperlipidemia, hypertension, smoking, alpha-tocopherol and
beta-carotene at baseline. The s-Se was not associated with
hsCRP, SAA or IL-6 at follow-up. In conclusion, high
concentrations of s-Se predict reduced levels of oxidative
stress and subclinical COX-mediated (but not
cytokine-mediated) inflammation in a male population. The
associations between Se, oxidative stress and inflammation,
respectively, might be related to the proposed
cardiovascular protective property of Se.
STATUS OF INTRACELLULAR AND
EXTRACELLULAR MAGNESIUM CONCENTRATION IN PATIENTS WITH
CARDIAC SYNDROME X.
Guo H., et al.
Acta Cardiol. 2005; 60(3):259-63.
This study sought to clarify
the differences of intracellular and extracellular
magnesium levels in patients with cardiac syndrome X.
Cardiac Syndrome X is defined as a typical angina
pectoris, positive treadmill exercise test, negatie IV
ergonovine test, and normal coronary angiography. The
researchers evaluated the intracellular and
extracellular magnesium status of 22 patients with
cardiac syndrome X (group A) and 22 age-and
gender-matched disorder-free control subjects (group B).
Levels of magnesium were determined in serum, urine,
erythrocytes, and the 24-h magnesium retention rate was
calculated by a magnesium loading test. Group A showed a
higher 24-h magnesium retention rate (49.8 +/- 1.3% vs.
32.6 +/- 7.5%, P < 0.05) and a lower intracellular
concentration of magnesium in erythrocytes than group B
(3.7 +/- 1.4 vs. 5.6 +/- 1.3 fg/cell, P < 0.05),
demonstrating the presence of magnesium deficiency in
qroup A. There were no significant differences in the
serum concentration of magnesium between groups A and B
(0.87 +/- 0.23 vs. 0.83 +/- 0.15 mmol/l).
The researchers concluded that this study demonstrated
that the intracellular magnesium level decreased in
patients with cardiac syndrome X.
ZINC DEFICIENCY INCREASES PLASMA
LIPIDS AND ATHEROSCLEROTIC MARKERS IN LDL-RECEPTOR-DEFICIENT
MICE.
Reiterer G, et al.
J Nutr 2005; 135(9):2114-8.
Low zinc concentration can
be associated with an increased risk of cardiovascular
diseases. In the current study, we hypothesize that zinc
deficiency can increase and zinc supplementation can
decrease proatherosclerotic events in LDL receptor
knock-out (LDL-R-I-) mice fed a moderate-fat diet. Mice
were fed either a zinc-deficient (0 micromol Zn/g), a
control (0.45 micromol Zn/g), or a zinc-supplemented
(1.529 micromol Zn/g) diet for 4 wk. Mice fed the zinc-
deficient diet had significantly increased
concentrations of cholesterol and triacylglycerides in
the VLDL and HDL fractions. Zinc supplementation
decreased these lipid variables compared with control
mice. We detected significantly higher concentrations of
glutathione reductase mRNA in the thoracic aortae of
zinc-deficient mice. Furthermore, inflammatory markers,
such as nuclear factor-kappaB and vascular cell adhesion
molecule-1, were significantly increased in
zinc-deficient mice compared with mice of the control or
supplemented groups. In addition, zinc deficiency
significantly reduced the DNA binding activity of
peroxisome proliferator activate receptors (PPARs) in
liver extracts. Interestingly, mRNA expression levels of
PPARgamma were significantly increased in thoracic
aortae of zinc-deficient mice, indicating an adaptation
process to decreased PPAR signaling. These data provide
in vivo evidence of zinc deficiency inducing
proinflammatory events in an atherogenic mouse model.
These data also suggest that adequate zinc may be a
critical component in protective PPAR signaling during
atherosclerosis.
MARGINAL DIETARY COPPER RESTRICTION
INDUCES CARDIOMYOPATHY IN RATS.
Li Y, et al.
J Nutr 2005; 135(():2130-6.
Prior studies have provided
evidence of marginal dietary copper restriction in humans.
The present study was undertaken to examine in a rat model
the effect of a long-term marginal dietary Cu deficiency on
the heart. Male adult Sprague-Dawley rats were fed AIN-76
diet containing 6.0 (control), 3.0, or 1.5 mg Cu/kg starting
at 11 wk of age. Groups of rats were killed at 6, 9, 12, 15,
or 18 mo after initiation of feeding, and the same
experiment was repeated once. The only systemic change
induced by marginal dietary Cu restriction (P < 0.05) was
depression of organ Cu concentrations in rats fed 1.5 mg
Cu/kg diet. Cardiac pathological manifestations in rats fed
lower Cu diets were evidenced by histopathological,
ultrastructural, and functional alterations. Myocyte
hypertrophy and excessive collagen deposition in the heart
occurred in rats fed 1.5 mg Cu/kg diet. Ultrastructural
changes, including increased number and volume of
mitochondria along with disruption of cristae structure,
diastolic and systolic dysfunction, and electrocardiograph
alterations, occurred in rats fed 1.5 or 3.0 mg Cu/kg diet.
These results demonstrate that, in the absence of most
indications of systemic Cu deficiency, heart morphology and
function are sensitive to marginal Cu deficiency .
IRON STATUS AND CLINICAL OUTCOME IN
PATIENTS WITH CORONARY ARTERY DISEASE AFTER CORONARY
STENTING
Ndrepepa G, et al.
Nutr Metab Cardiovasc Dis, 2005; 15(6):418-25.
So far, no studies have assessed whether there is an
association between iron status and the incidence of major
adverse cardiac events or restenosis after coronary stenting.
We conducted this study to investigate whether there is an
association between body iron status and clinical outcome in
patients with coronary artery disease after coronary
stenting. The study included 664 patients with coronary
artery disease who underwent coronary stent implantation.
The soluble transferring receptor/ferritin ratio (sTfR/ferritin
ratio) was used as an index of iron status. Patients were
divided into three groups according to the tertiles of sTfR/ferritin
ratio: lower tertile (11.9; n=221), middle tertiIe
(11.9-27.8; n=221) and upper tertile (>27.8; n=222). The
combined incidence of major adverse cardiac events (death,
myocardial infarction and target vessel revascularization)
was the primary end point of the study. Patients in the
lower tertile of the sTfR/ferritin ratio presented more
often with unstable angina or acute myocardial infarction
and had longer lesions and higher grade of stenosis than the
patients in the middle or upper tertile of the sTfR/ferritin
ratio. Angiographic restenosis at 6-month angiography was
also evaluated. The cumulative event rate of composite end
point of death, myocardial infarction or target vessel
revascularization was 27.6% in patients in the lower tertile,
24.4% in patients in the middle tertile and 28.4% in
patients in the upper tertile of the sTfR/ferritin ratio
(p=O.68). Restenosis was found in 27.8% (n=45) in the lower
tertile, 25.8% (n=42) in the middle tertile and 27.5% (n=38)
in the upper tertile of the sTfR/ferritin ratio (p=O.90).
The study showed no association between iron status and the
incidence of major adverse cardiac events or angiographic
coronary restenosis in patients with coronary artery disease
after coronary stenting.
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