(HOME) Subject: crohn
Subject: crohn
Proc Natl Acad Sci U S A 1996 Sep 3;93(18):9816-20
On the etiology of Crohn disease.
Mishina D, Katsel P, Brown ST, Gilberts EC, Greenstein RJ
Laboratory of Molecular Surgical Research, Veterans Affairs Medical
Center, Bronx, NY 10468, USA.
Crohn disease (CD) is a chronic, panenteric intestinal inflammatory
disease. Its etiology is unknown. Analogous to the tuberculoid and
lepromatous forms of leprosy, CD may have two clinical manifestations.
One is aggressive and fistulizing (perforating), and the other is
contained, indolent, and obstructive (nonperforating) [Gi]-berts, E.
C. A. M., Greenstein, A. J., Katsel, P., Harpaz, N. & Greenstein, R.
J. (1994) Proc. Natl. Acad. Sci. USA 91, 12721-127241. The etiology,
if infections, may be due to Mycobacterium paratuberculosis. We
employed reverse transcription PCR using M. paratuberculosis
subspecies-specific primers (IS 900) on total RNA from 12 ileal
mucosal specimens (CD, n = 8; controls, n = 4, 2 with ulcerative
colitis and 2 with colonic cancer). As a negative control, we used
Myobacterium avium DNA, originally cultured from the drinking water of
a major city in the United States. cDNA sequence analysis shows that
all eight cases of Crohn's disease and both samples from the patients
with ulcerative colitis contained M. paratuberculosis RNA.
Additionally, the M. avium control has the DNA sequence of M.
paratuberculosis. We demonstrate the DNA sequence of M.
paratuberculosis from mucosal specimens from humans with CD. The
potable water supply may be a reservoir of infection. Although M.
paratuberculosis signal in CD has been previously reported, a cause
and effect relationship has not been established. In part, this is due
to conflicting data from studies with empirical antimycobacterial
therapy. We conclude that clinical trials with anti-M.
paratuberculosis therapy are indicated in patients with CD who have
been stratified into the aggressive (perforating) and contained
(nonperforating) forms.
PMID: 8790414, UI: 96382550
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Subject: sepsis/ph
Microb Pathog 1993 Mar;14(3):229-38
Inability to detect mycobactin in mycobacteria-infected tissues suggests an
alternative iron acquisition mechanism by mycobacteria in vivo.
Lambrecht RS, Collins MT
Department of Health Sciences, University of Wisconsin-Milwaukee,
53211.
Although most species of mycobacterium are capable of producing
mycobactin, it is not known if conditions within the host allow for
mycobactin synthesis or whether it even plays a role in iron
acquisition in vivo. We employed the mycobactin-auxotroph,
Mycobacterium paratuberculosis, in a bioassay to examine tissues from
animals infected with either Mycobacterium tuberculosis, Mycobacterium
avium or M. paratuberculosis for the presence of mycobactin or
compounds which demonstrate mycobactin-like activity. Other
iron-binding compounds, including purified siderophores from unrelated
organisms and host iron-binding proteins were also evaluated in the
bioassay for growth induction of M. paratuberculosis in the absence of
mycobactin. Although mycobactin could be easily demonstrated in
tissues artificially seeded with mycobacteria, no mycobactin could be
detected in heavily infected tissues. None of the purified
siderophores from unrelated microorganisms were found to support
growth of M. paratuberculosis in the absence of mycobactin. Host
iron-binding proteins (transferrin, lactoferrin, ferritin, hemin) also
failed to induce growth in the bioassay at pH 6.8, however, when the
pH was adjusted between 5-6.2, transferrin and lactoferrin promoted
growth of M. paratuberculosis without mycobactin, probably as a result
of the dissociation of iron rather than a specific interaction. We
confirm that mycobacteria are incapable of iron uptake when iron is
chelated to siderophores from unrelated organisms and conclude that
mycobactin-mediated mechanisms of iron-acquisition by mycobacteria do
not appear to have as significant a role in vivo as in vitro. In
addition, evidence is presented that suggests iron-containing
transferrin and lactoferrin at low pH may circumvent the need for
mycobactin by M. paratuberculosis.
PMID: 8321124, UI: 93309299
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Subject: Iron and bacteria
J Clin Invest 61: 1428-40 (1978)[78194498]
The critical role of iron in host-bacterial interactions.
S. M. Payne & R. A. Finkelstein
The ability of potential pathogens to acquire iron in a host is an
important determinant of both their virulence and the nature of the
infection produced. Virulent gram-negative bacteria are capable of
acquiring sufficient iron from the host because their virulence (for
chick embryos) is unaffected by exogenous iron. Avirulent mutants
which are apparently limited in their ability to acquire iron could be
isolated from the virulent strains. The lethality of these mutants was
significantly enhanced by exogenous iron. Reduction of the relatively
high serum iron saturation of chick embryos (to levels more closely
approximating those in man) by pretreatment with iron-binding proteins
or endotoxin inhibits the lethality of some virulent bacteria. Those
bacteria whose virulence was reduced include the Shigella, Vibrio
cholerae and strains of Neisseria gonorrhoeae, all of which are
nondisseminating pathogens in the normal human host. Pathogens which
produce septicemic and disseminating infections such as Neisseria
meningitidis, Haemophilus influenzae type B, Escherichia coli
possessing K-1 antigen, Pseudomonas aeruginosa and Salmonella
typhimurium and disseminating strains of N. gonorrhoeae were, in
general, unaffected by reduced serum iron saturation. These
disseminating bacteria appeared to produce greater quantities of
compounds (siderophores) which stimulated microbial growth in low-iron
media than did the nondisseminating pathogens. Thus, the gram-negative
bacteria tested can be divided into four major classes according to
their responses to modifications in iron levels in the chick embryo
model and these results correlate with the nature of the infections
which they typically produce in man.
MeSH Terms:
* Animal
* Bacteria/drug effects
* Bacteria/metabolism
* Bacteria/pathogenicity
* Bacterial Infections/immunology
* Bacterial Infections/metabolism
* Chick Embryo
* Conalbumin/pharmacology
* Iron/metabolism
* Iron/pharmacology
* Iron Chelates/metabolism
* Support, U.S. Gov't, P.H.S.
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Ann Clin Lab Sci 2000 Oct;30(4):354-65
Effects of iron overload on the immune system.
Walker EM Jr, Walker SM
Department of Pathology, Marshall University and Huntington DVA
Medical Center, West Virginia, 25704, USA. walkere@marshall.edu
[Medline record in process]
Iron and its binding proteins have immunoregulatory properties, and
shifting of immunoregulatory balances by iron excess or deficiency may
produce severe, deleterious physiological effects. Effects of iron
overload include decreased antibody-mediated and mitogen-stimulated
phagocytosis by monocytes and macrophages, alterations in T-lymphocyte
subsets, and modification of lymphocyte distribution in different
compartments of the immune system. The importance of iron in
regulating the expression of T-lymphocyte cell surface markers,
influencing the expansion of different T-cell subsets, and affecting
immune cell functions can be demonstrated in vitro and in vivo. The
poor ability of lymphocytes to sequester excess iron in ferritin may
help to explain the immune system abnormalities in iron-overloaded
patients. Iron overload as seen in hereditary hemochromatosis patients
enhances suppressor T-cell (CD8) numbers and activity, decreases the
proliferative capacity, numbers, and activity of helper T cells (CD4)
with increases in CD8/CD4 ratios, impairs the generation of cytotoxic
T cells, and alters immunoglobulin secretion when compared to treated
hereditary hemochromatosis patients or controls. A correlation has
recently been found between low CD8+ lymphocyte numbers, liver damage
associated with HCV positivity, and severity of iron overload in
beta-thalassemia major patients. Iron overload, with its associated
increases of serum iron levels and transferrin saturation, may cause a
poor response to interferon therapy. Iron overload with hyperferremia
is associated with suppressed functions of the complement system
(classic or alternative types). High plasma ferritin content in
patients with chronic, diffuse diseases of the liver (cirrhosis,
chronic hepatitis), beta-thalassemia major, dyserythropoiesis, and
hereditary hemochromatosis may induce the development of anti-ferritin
antibodies with the production of circulating immune complexes.
Increased body stores of iron in various clinical situations may tip
the immunoregulatory balance unfavorably to allow increased growth
rates of cancer cells and infectious organisms, and complicate the
clinical management of preexisting acute and chronic diseases.
PMID: 11045759, UI: 20498458
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Subject: phytic acid/antioxidant/chelator
Protective Effect of Phytic Acid Hydrolysis Products on Iron-Induced
Lipid Peroxidation of Liposomal Membranes, Sayuri Miyamotoa, Goro
Kuwatab, Masatake Imaib, Akihiko Nagaoc, and Junji Teraoa,*,
aDepartment of Nutrition, School of Medicine, The University of
Tokushima, Tokushima 770-8503, Japan, bResearch Institute of Morinaga
& Co. Ltd., Yokohama 230-0012, Japan, and cNational Food Research
Institute, Ministry of Agriculture, Forestry and Fisheries, Tsukuba
305-0856, Japan
Beneficial effects of dietary phytic acid (myo-inositol
hexaphosphate; IP6) have often been explained by its strong iron
ion-chelating ability, which possibly suppresses iron ion-induced
oxidative damage in the gastrointestinal tract. Because phytic acid is
hydrolyzed during digestion, this work aimed to know whether its
hydrolysis products (IP2, IP3, IP4, and IP5) could still prevent iron
ion-induced lipid peroxidation. Studies using liposomal membranes
demonstrated that hydrolysis products containing three or more
phosphate groups are able to inhibit iron ion-induced lipid
peroxidation although their effectiveness decreased with
dephosphorylation. Similarly, they also prevented iron ion-induced
decomposition of phosphatidylcholine hydroperoxide. These results
demonstrate that intermediate products of phytic acid hydrolysis still
possess iron ion-chelating ability, and thus they can probably prevent
iron ion-induced lipid peroxidation in biological systems
Paper no. L8625 in Lipids 35, 1411-1413 (December 2000).
Subject: phytic acid/Ip6
From The June 2000 Issue of Nutrition Science News
Feature
Too Much of a Good Thing
by Bill Sardi
Bioflavonoids (found in berries, coffee, green tea, pine bark,
quercetin and the rind of citrus fruits, particularly blueberry,
cranberry, elderberry and grape seed) and phytic acid (a component of
whole grains and seeds such as sesame) bind to iron and other minerals
in the gastric tract and help to limit iron availability. If
bioflavonoids and phytic acid haven't bound to minerals in the
digestive tract they will get into the bloodstream, where they can
bind to free iron, acting as blood-cleansing iron chelators.
Therefore, maximum iron chelation in the blood circulation is achieved
when these iron binders are consumed apart from meals.
Phytic acid--also called inositol hexaphosphate, or IP6--is comprised
of six phosphorus molecules and one molecule of inositol. It has been
mistakenly described for decades as an "anti-nutrient" because it
impairs mineral absorption. However, in the 1980s food biochemist
Ernst Graf, Ph.D., began to tout phytic acid for its beneficial
antioxidant properties achieved through mineral chelation.32
Phytic acid in foods or bran should be distinguished from supplemental
phytic acid, which is derived from rice bran extract. In foods, phytic
acid binds to iron and other minerals in the digestive tract and may
interfere with mineral absorption. As a purified extract of rice bran,
taken between meals so it will not bind to minerals in the digestive
tract, phytic acid is readily absorbed into the bloodstream, where it
acts as a potent mineral chelator.33 Phytic acid binds to any free
iron or other minerals (even heavy metals such as mercury, lead and
cadmium) in the blood, which are then eliminated through the kidneys.
Phytic acid removes only excess or unbound minerals, not mineral ions
already attached to proteins.
Phytic acid is such a potent--but safe--iron and mineral chelator that
it may someday replace intravenous chelation therapy such as the
mineral-chelator EDTA or iron-binding drugs such as desferrioxamine
(Desferal). Because of its ability to bind to iron and block
iron-driven hydroxyl radical generation (water-based) as well as
suppress lipid peroxidation (fat-based), phytic acid has been used
successfully as an antioxidant food preservative.34
Phytic acid supplements should not be taken during pregnancy since the
developing fetus requires minerals for proper development. Because
aspirin causes a small loss of blood and consequently helps to control
iron levels, the simultaneous use of phytic acid with a daily aspirin
tablet is not advised. A three-month course of phytic acid should
achieve adequate iron chelation, and prolonged daily supplementation
may lead to iron-deficiency anemia. Anemic individuals who take phytic
acid as a food supplement are likely to feel weak shortly after
consumption, whereas iron-overloaded individuals are likely to feel
increased energy.
For those at risk for iron overload, it may be wise to avoid iron in
multivitamins and shun fortified foods that provide more than 25
percent of the recommended daily intake for iron. No doctor should
prescribe iron tablets for patients who complain of fatigue without
blood tests and a thorough health history. Iron-rich foods such as red
meat and molasses may prevent anemia and build strength during the
growing years but in adulthood may lead to iron overload among men and
postmenopausal women. Those individuals who learn how to achieve iron
balance will maintain the most desirable state of health throughout
life.
Subject: bacteria/iron
Clin Microbiol Rev 1996 Oct;9(4):435-447
Mycobacterium haemophilum: microbiology and expanding clinical and geographic
spectra of disease in humans.
Saubolle MA, Kiehn TE, White MH, Rudinsky MF, Armstrong D
Department of Pathology, Good Samaritan Regional Medical Center,
Phoenix, Arizona 85006, USA.
Reports of the association of Mycobacterium haemophilum with disease
in humans have greatly increased. At least 64 cases have now been
reported, with symptoms ranging from focal lesions to widespread,
systemic disease. The organism is now known to cause primarily
cutaneous and subcutaneous infection, septic arthritis, osteomyelitis,
and pneumonitis in patients who are immunologically compromised and
lymphadenitis in apparently immunocompetent children. Underlying
conditions in the compromised patients have included AIDS; renal, bone
marrow, and cardiac transplantation; lymphoma; rheumatoid arthritis;
marrow hypoplasia; and Crohn's disease. Reports have originated from
diverse geographic areas worldwide. The epidemiology of M. haemophilum
remains poorly defined; there appears to be a genetic diversity
between strains isolated from different regions. The organism is
probably present in the environment, but recovery by sampling has not
been successful. M. haemophilum has several unique traits, including
predilection for lower temperatures (30 to 32 degrees C) and
requirement for iron supplementation (ferric ammonium citrate or
hemin). These may in the past have compromised recovery in the
laboratory. Therapy has not been well elucidated, and the outcome
appears to be influenced by the patient's underlying
immunosuppression. The organisms are most susceptible to
ciprofloxacin, clarithromycin, rifabutin, and rifampin. Timely
diagnosis and therapy require communication between clinician and the
laboratory.
Publication Types:
* Review
* Review, academic
PMID: 8894345, UI: 97049617
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____ the above report in [Macintosh] [Text] format
_____ documents on this page through Loansome Doc
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Subject: zinc/diarrhea
> Zinc Supplements Important In Combating Diarrhea
http://www.pslgroup.com/dg/1ec252.htm
Researchers have found that zinc supplements help
children suffering from acute and persistent
diarrhea significantly reduce the duration of their
symptoms.
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Zinc Supplements Important In Combating Diarrhea
BALTIMORE, MD -- November 28, 2000 -- Researchers at the Johns Hopkins
School of Public Health have found that zinc supplements help children
suffering from acute and persistent diarrhea significantly reduce the
duration of their symptoms. The study can be found in the December
2000 issue of the American Journal of Clinical Nutrition.
"Diarrhea is a very serious public health problem in developing
countries, resulting in millions of deaths each year. Those who
survive are often left with malnutrition. This study was important
because it measures the effect of supplemental zinc given in
conjunction with oral rehydration therapy during the recovery from
acute or persistent diarrhea," said study co-coordinator Robert Black,
MD, MPH, professor and chair, International Health, Johns Hopkins
School of Public Health.
The researchers analyzed ten randomized, controlled studies that had
assessed the therapeutic benefit of zinc supplements in children under
age five. In the case of the acute-diarrhea trials, diarrhea was
defined as three or four loose stools in a 24-hour period. For
persistent diarrhea, the original trials' definitions for diarrhea and
recovery were retained.
All trials used the standard World Health Organization recommendations
for fluid and dietary case management of diarrhea. The researchers
divided the participants of all the reviewed studies into subgroups
according to sex, age, weight-for-height, and initial plasma zinc
concentration, and then evaluated the overall effect of zinc on each
group.
Results of the study showed that the children who were given a zinc
supplement during the acute-diarrhea trials were 15 percent less
likely than controls to still have diarrhea by a given day; children
in the persistent-diarrhea trials had a 24 percent lower risk of the
diarrhea continuing. The authors said their meta-analysis showed that
zinc apparently offers comparable benefits to all subgroups, a finding
that indicates the nutrient needn't be aimed only at certain narrow
populations but is feasible for wide use in the developing world.
Although future studies are still needed to examine the effect of zinc
supplementation on other measures of severity, such as diarrheal
output, occurrence of dehydration, treatment failure, or death, the
researchers believe attention should now focus on the best means of
providing zinc during diarrhea, as well as on other ways to increase
the zinc intake of children in developing countries.
This study was supported by the Johns Hopkins Family Health and Child
Survival Cooperative Agreement with the U.S. Agency for International
Development, by the World Health Organization's Division of Child
Health and Development, and by the Rockefeller Foundation's Bellagio
Study and Conference Center.
Clin Gastroenterol 12: 713-41 (1983)[84002834]
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Clin Gastroenterol 12: 713-41 (1983)[84002834]
The role of zinc in gastrointestinal and liver disease.
A. S. Prasad
Zinc is essential for many metabolic and enzymatic functions in man.
Deficiency of zinc in man has now been recognized to occur not only as
a result of nutritional factors, but also in various disease states,
including malabsorption syndromes, acrodermatitis enteropathica,
Crohn's disease, alcoholism and cirrhosis of the liver. The deficiency
state in human subjects exists as a spectrum extending from mild to
severe degree. The clinical manifestations of mild zinc deficiency
include oligospermia, weight loss and hyperammonaemia. Moderate zinc
deficiency is characterized clinically by growth retardation,
hypogonadism in males, skin changes, poor appetite, mental lethargy,
delayed wound healing, taste abnormalities and abnormal dark
adaptation. In severe zinc deficiency states, bullous-pustular
dermatitis, alopecia, diarrhoea, emotional disorders, weight loss,
intercurrent infections, hypogonadism in males and, if unrecognized,
death have been observed. Zinc is needed for the functions of over 100
enzymes. It is essential for DNA, RNA and protein synthesis and, as
such, is important for cell division. Zinc is an inducer of mRNA of
metallothionein, a protein which may have an important role in the
regulation of intestinal zinc absorption. Zinc has a specific effect
on testes in animals and man. Recent reports indicate that in human
subjects thymopoietin may be zinc dependent and in animal studies
somatomedin may be affected adversely due to dietary zinc restriction.
Zinc plays an important role in the protection of cell membrane
integrity and may be protective against free radical injury. Zinc is
known to compete with cadmium, lead, copper, iron and calcium for
similar binding sites. In the future, a potential use of zinc may be
to alleviate toxic effects of cadmium and lead in human subjects.
Recent evidence suggests that thymic-dependent lymphocytes (T cells
are zinc dependent. T-helper and suppressor cells, T-effector cells
and T-natural killer cells appear to be zinc dependent. Zinc is also
essential for some of the neutrophil functions. Thus, it appears that
zinc may play an important role in immunity. One may suggest that some
of the clinical features of cirrhosis of the liver, such as testicular
atrophy, loss of body hair, night blindness, poor wound healing, poor
appetite, susceptibility to infections and enhanced sensitivity to
drugs, may be related to conditioned deficiency of zinc, future
studies are required to determine whether or not zinc supplementation
is beneficial to these patients.
MeSH Terms:
* Acrodermatitis/metabolism
* Adult
* Alcoholism/metabolism
* Cell Cycle
* Cell Membrane/metabolism
* Collagen/metabolism
* Female
* Gastrointestinal Diseases/metabolism
* Hormones/metabolism
* Human
* Liver Diseases/metabolism
* Male
* Nucleic Acids/metabolism
* Support, U.S. Gov't, P.H.S.
* Zinc/deficiency
* Zinc/physiology
Substances:
* Collagen
* Zinc
* Nucleic Acids
* Hormones
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Subject: iron studies/anemia/Iran/zinc
Haghshenass M, Mahloudji M, Reinhold J, et al., "Iron-deficiency
Anemia in an Iranian Population Associated with High Intakes of Iron",
(Nov 1972), The American Journal of Clinical Nutrition, 25 (11), pp:
1143-6.
Yip R, Reeves JD, Lonnerdal B, et al., "Does Iron Supplementation
Compromise Zinc Nutrition in Healthy Infants?", (Oct 1985), The
American Journal of Clinical Nutrition, 42 (4), pp: 683-7.
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J. Biol. Chem. 271: 5125-5130 (1996)[96214945]
In vivo and in vitro iron-replaced zinc finger generates free radicals and
causes DNA damage.
D. Conte, S. Narindrasorasak & B. Sarkar
Department of Biochemistry Research, The Hospital for Sick Children,
Toronto, Ontario M5G 1X8, Canada.
The estrogen receptor (ER) is a ligand-activated transcription factor
whose DNA-binding domain (ERDBD) has eight cysteines, which coordinate
two zinc atoms, forming two zinc finger-like structures. We
demonstrate the capability of iron to replace zinc in zinc finger
(hereby referred to as iron finger) both in vivo (using Escherichia
coli BL21 (DE3)) and in vitro. Iron has the ability to substitute for
zinc in the ERDBD as demonstrated by mobility shift and methylation
interference assays of iron finger, which show specific recognition of
the estrogen response element. The DNA binding constants for both in
vivo and in vitro iron-replaced zinc fingers were similar to that of
the native finger. Atomic absorption analysis revealed a ratio of 2:1
iron atoms/mol of ERDBD protein, as found for zinc in the crystal
structure of native ERDBD. More importantly, we demonstrate that iron
finger in the presence of H2O2 and ascorbate generates highly reactive
free radicals, causing a reproducible cleavage pattern to the
proximate DNA, the estrogen response element. The deoxyribose method,
used to detect free radical species generated, and the resultant
cleaved DNA ends, caused by iron finger, suggest that the free
radicals generated are hydroxyl radicals. Due to the close proximity
of the zinc finger to DNA, we postulate that iron-substituted zinc
finger may generate free radicals while bound to genetic regulatory
response elements, leading to adverse consequences such as
iron-induced toxicity and/or carcinogenesis.
MeSH Terms:
* Base Sequence
* Cloning, Molecular
* Comparative Study
* DNA Damage*
* DNA-Binding Proteins/metabolism
* DNA-Binding Proteins/biosynthesis
* DNA, Bacterial/metabolism
* DNA, Bacterial/chemistry
* Escherichia coli/metabolism
* Escherichia coli/growth & development
* Free Radicals/metabolism
* Human
* Iron/pharmacology
* Kinetics
* Methylation
* Models, Molecular
* Molecular Sequence Data
* Nucleic Acid Conformation
* Oligodeoxyribonucleotides
* Protein Structure, Secondary
* Receptors, Estrogen/metabolism
* Receptors, Estrogen/biosynthesis
* Recombinant Proteins/metabolism
* Recombinant Proteins/biosynthesis
* Support, Non-U.S. Gov't
* Time Factors
* Zinc/physiology
* Zinc Fingers*
Substances:
* Zinc
* Iron
* Recombinant Proteins
* Receptors, Estrogen
* Oligodeoxyribonucleotides
* Free Radicals
* DNA, Bacterial
* DNA-Binding Proteins
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Subject: zinc/iron
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Effects of Trace Elements Supplementation on Measures of Nutritional Status
Effects of supplementation with zinc (30.4 mg/d), copper (3.4 mg/d),
and chromium (241 ug/d) on alkaline phosphatase, serum ferritin,
hemoglobin, and plasma and erythrocyte copper, iron, and zinc were
examined in apparently healthy adults over the age of 50. Differences
were found between males and females within supplement groups. Serum
ferritin decreased significantly during and following zinc
supplementation in males. Total hemoglobin increased significantly
from baseline to four weeks post supplementation in chromium and
copper supplemented females. Alkaline phosphatase decreased from
baseline to four weeks post supplementation in all groups. The
decrease was significant in the mineral supplement groups except for
females receiving zinc--but not in the placebo group. Plasma zinc
increased significantly in zinc supplemented males and during
supplementation and in copper supplemented females from the end of
supplementation to four weeks post supplementation. In the copper
group, plasma copper decreased during supplementation in females but
was not significantly different over time in males, while in the
chromium supplemented females plasma copper increased at eight weeks
of supplementation. These results support the importance of examining
the interactive effects of minerals in both males and females.
Sponsor: Agricultural Experiment Station
PI: Andrea Arquitt
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