Boron Deprivation Increases Plasma
Homocysteine, a Factor Negatively Associated with Bone
Composition and Strength
Forrest H. Nielsen.
The FASEB journal 2007;21 :2144.5
Boron (B) deprivation decreases trabecular bone in
vertebrae of rats. Elevated plasma homocysteine (HCY) has
been associated with decreased trabecular bone. It has been
observed that S-adenosylmethionine, an, intermediate in the
formation of Hcy, has the highest known affinity for boron
of mammalian compounds examined to date. In view of this,
the effect of boron deprivation on plasma Hcy and cysteine (Cys)
was determined. Dietary n-3 fatty acids can affect the
response to B deprivation and decrease plasma Hcy. Female
weanling rats were fed diets containing 75 g of corn oil/kg
and 0.1 (B-def) or 3.1 (B-adq) mg B/kg then bred. After
weaning 60 male pups were divided into two groups. One group
continued on the diets fed their mothers, while the second
group was fed diets containing 0.1 or 3.1 mg B/kg plus 65 g
fish oil/kg and 10 g linoleic acid/kg. Plasma and femurs
were collected at 18 weeks. Boron deficiency was confirmed
by decreased femur B and B-deficient responses of decreased
femur iron and magnesium. Boron deficiency
increased plasma Hcy, and both boron deficiency and corn oil
versus fish oil increased plasma Cys. Boron deficient rats
fed corn oil had the highest plasma Cys. This group also had
the lowest calcium and the highest copper concentration in
the femur. These findings suggest that boron and n-3 fatty
acids impact sulfur amino acid metabolism differently.
Changes in cysteine related metabolic pathways could be, at
least in part, responsible for the interaction between boron
and dietary oil affecting bone composition.
Effectiveness of Different Iron
Supplementation Strategies on Hemoglobin and Ferritin Levels
Among Schoolchildren in Teresina, Piauí State, Brazil
Cad Saude Publica ; 2007; 23(7):1547-52.
Dos Santos MM ; Nogueira Ndo N ; Diniz Ada S.
This study evaluated the effectiveness of
supplementation with ferrous sulfate and iron bis-glycinate
chelate on hemoglobin and serum ferritin levels among
schoolchildren (7-11 years) of both sexes. A randomized
community-based trial including 138 anemic children
(hemoglobin < 11.5 g/dL) was conducted in Teresina, Piauí
State, Brazil. Children were assigned to two treatment
groups on an individual basis. One group (n = 71) received
40 mg iron as ferrous sulfate once weekly and the other
group (n=67) received 3.8 mg of iron bis-glycinate chelate-enriched
cookies, 3x/week, for 8 weeks. The interventions showed a
significant increase (p < 0.01) in hemoglobin levels (1.1 g/dL)
for children who received ferrous sulfate and 0.9 g/dl in
those who received iron bis-glycinate chelate, although not
significant in the inter-group comparison p > 0.05). No
effect was observed on body iron for either intervention (p
>
0.05). Children with depleted iron stores (15 ng/mL) at the
beginning of interventions showed increased serum ferritin
concentrations after 8 weeks (p < 0.01), although no
difference between treatments (p > 0.05) was observed. The
results confirm the effectiveness of the iron
supplementation interventions and corroborate the use of
iron salts or ferrous bisglycinate chelate on a weekly basis
to overcome iron deficiency and anemia.
Copper Deficiency Decreases Plasma
Homocysteine in Rats
Uthus EO ; Reeves PG ;
Saari JT.
J Nutr; 2007; 137(6):1370-4.
The purpose of this study was to determine the effects of
copper deficiency on key aspects of homocysteine metabolism
that involve methionine recycling and transsulfuration, Male
weanling Sprague-Dawley rats were fed AIN-93G-based diets
containing <1 or approximately 6 mg Cu/kg. After 6 wk (Expt.
1) and 4 wk (Expt. 2) we found that plasma homocysteine was
significantly decreased, and plasma glutathione
significantly increased, in rats fed the low-Cu diet.
Real-time RT-PCR was used to determine the expression of the
subunits of glutamatecysteine ligase (Gcl) in liver that
catalyzes the rate-limiting step in glutathione
biosynthesis. The expression of Gclc, the catalytic subunit
of Gcl, was upregulated by Cu deficiency; Gclm, the modifier
subunit, was not affected. Hepatic betainehomocysteine
methyltransferase (Bhmt), which catalyzes one of the two
ways that homocysteine can be remethylated to methionine,
was downregulated by Cu deficiency. Because Cu deficiency
results in upregulation of Gclc and an increase in the
biosynthesis of glutathione, it is plausible that the net
flux of homocysteine through the transsulfuration pathway is
increased. Furthermore, if Bhmt is downregulated, less
homocysteine is available for remethylation (methionine
recycling) and more is then available to irreversibly enter
the transsulfuration pathway where it is lost. The net
effect of increased Gclc and decreased Bhmt would be a
decrease in homocysteine as a result of Cu deficiency.
Zinc Deficiency
Depresses Red Cell Production in Rats
Konomi A; Katsubiko Y.
FASEB; 2007; 21:697-3.
Zinc (Zn) deficiency occurs worldwide and a very important
public health problem. To investigate the physiological role
of Zn in hematopoiesis, forty 4-week-old male Sprague-Dawley
rats were assigned into 3 dietary treatment groups of 10 for
the 4-week study: Control group (AIN-93G; Cont),
Zn-deficient group (4.5 mg Zn/kg; ZD) and pair-fed group
(AIN-93G; PF). Body water distribution was measured by a
bioimpedance analyzer. Complete blood counts, reticulocyte
(Ret) and red cell distribution width (RDW/SD) were measured
by an electronic counter. Plasma erythropoietin (EPO)
concentration was determined by ELISA. Alkaline phosphatase
(ALP) activity was measured by the colorimetric kit.
Statistical analysis was performed by PLSD. Hgb was
significantly different between all groups. Hgb and RDW /SD
of ZD were significantly higher than PF. Ret of ZD was
significantly lower than Cont (P<O.O I) indicating decreased
erythropoiesis. RDW /SD and MCV of ZD were significantly
higher than Cont (P<O.OI and P<O.05 respectively). Plasma
ALP of ZD was significantly lower than Cont and PF. Plasma
EPO of ZD was significantly lower than Cont (P<O.05). These
results suggest that Zn deficiency induces impaired EPO
production and erythropoiesis associating macrocytosis and
anisocytosis revealed by blood smear as well.
Exercise-induced Suppressed Reactivity of T-lymphocyte
was Improved By
Zinc Supplementation in Athletes
Okhee L, and Hyun-Sook Lee.
FASEB; 2007; 21:604.10.
Athletes are exposed to acute and chronic stress
that may lead to suppression of the immune system and
increased oxidative species generation. Normal Zn levels
are essential for the development and maintenance of
immune functions. We examined whether the Zn
supplementation attenuate the exercise-induced changes
in immunity. Female basketball players (n = 12), aged
19~26 years, were supplemented with Zn (Zn glycerate, Zn
50 mg) for 8 weeks. Before and after Zn intervention,
they exercised in treadmill until exertion according to
Bruce protocol. We collected the blood of the subjects
before and after exercise and Zn supplementation. The
proportion of immune cell in blood such as neutrophil,
monocyte, eosinophile, and lymphocytes were
significantly decreased after exercise (p < 0.01).
Concanavalin A (ConA) - or phytohematogglutinin (PHA) -
induced lymphocyte proliferations were significantly
decreased after exercise. However, lipopolysaccharide
(LPS) - induced lymphocyte proliferation was not
significantly affected by exercise. After Zn
supplementation, the proprotion of neutrophil, monocyte,
and lymphocyte in WBC except eosinophil were not
different. ConA- or PHA-induced lymphocyte proliferation
rate were less diminished when the subject had exercised
after Zn supplementation (p < 0.01). However, Zn
supplementation did not affect the
LPS-induced lymphocyte proliferation. These results
suggest that exercise-induced oxidative stress decrease
the T cell function compared to B cell. And Zn
supplementation to the athletes with normal Zn
nutritional status has a positive effect on
exerciseinduced change in immune function, especially
T-cell function.
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