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Title
zinc administration prevents wasting in stressed mice.
Author
Garc]ia Tamayo F; Terrazas Vald]es LI; Malpica L]opez N
Address
Departamento de Biolog]ia' Facultad de Qu]imica' Universidad
Nacional
Aut]onoma de M]exico' M]exico' D.F.
Source
Arch Med Res, 27(3):319-25 1996 Autumn
Abstract
Experimentally induced chronic stress can produce severe retardation
on
the physical development of young animals. Moreover' the chronic
stress
and its associated secondary malnutrition cause a variable depression
on immunity' whose pathogenesis has been related to the excessive
production of cytokines and glucocorticoids. When stressful stimuli
are
excessive' animals increment their anorexia and express a progressively
installed wasting syndrome' associated with hypozincemia and
susceptibility to infections with high mortality rate. In this
work'
chronically stressed mice were studied to observe the prophylactic
effect of a zinc treatment on the evolution of both their malnutrition
and their immune competence. Stress was induced in newborn Balb/c
mice
by intraperitoneal (IP) inJections with heat-killed bacteria
for 4
weeks. Following this inductive period' almost all the stressed
mice
showed a transient wasting syndrome characterized by anorexia'
deficient gain of corporal weight' diarrhea' skin infection'
reduced
antibody response against antigens of red blood sheep cells'
and a
decreased proliferative response in their Con-A stimulated splenic
lymphocytes. However' when the stressed mice received an additional
IP
treatment with zinc acetate' their clinical condition showed
a
significant improvement and their immunocompetence was similar
to that
exhibited by non-stressed mice from the control groups. The results
suggest that zinc supplementation can ameliorate the effects
of chronic
stress on the growth' corporal weight' and immunocompetence of
young
mice.
Title
Integrated defense system overlaps as a disease model: with examples
for multiple chemical sensitivity.
Author
Rowat SC
Address
Grantham's Landing, British Columbia, Canada. steven_rowat@sunshine.net
Source
Environ Health Perspect, 106 Suppl 1():85-109 1998 Feb
Abstract
The central nervous, immune, and endocrine systems communicate
through
multiple common messengers. Over evolutionary time, what may
be termed
integrated defense system(s) (IDS) have developed to coordinate
these
communications for specific contexts; these include the stress
response, acute-phase response, nonspecific immune response,
immune
response to antigen, kindling, tolerance, time-dependent sensitization,
neurogenic switching, and traumatic dissociation (TD). These
IDSs are
described and their overlap is examined. Three models of disease
production are generated: damage, in which IDSs function incorrectly;
inadequate/inappropriate, in which IDS response is outstripped
by a
changing context; and evolving/learning, in which the IDS learned
response to a context is deemed pathologic. Mechanisms of multiple
chemical sensitivity (MCS) are developed from several IDS disease
models. Model 1A is pesticide damage to the central nervous system,
overlapping with body chemical burdens, TD, and chronic zinc
deficiency; model 1B is benzene disruption of interleukin-1,
overlapping with childhood developmental windows and hapten-antigenic
spreading; and model 1C is autoimmunity to immunoglobulin-G (IgG),
overlapping with spreading to other IgG-inducers, sudden spreading
of
inciters, and food-contaminating chemicals. Model 2A is chemical
and
stress overload, including comparison with the
susceptibility/sensitization/triggering/spreading model; model
2B is
genetic mercury allergy, overlapping with: heavy metals/zinc
displacement and childhood/gestational mercury exposures; and
model 3
is MCS as evolution and learning. Remarks are offered on current
MCS
research. Problems with clinical measurement are suggested on
the basis
of IDS models. Large-sample patient self-report epidemiology
is
described as an alternative or addition to clinical biomarker
and
animal testing.
Title
Age-associated problems in nutrition.
Author
Sone Y
Address
Department of Food and Nutrition' Faculty of Human Life Science'
Osaka
City University.
Source
Appl Human Sci, 14(5):201-10 1995 Sep
Abstract
From the chapters described so far' it is apparent that human
beings
may suffer many kinds of physiological declines during aging
process.
However' nutritional problems due to the physiological declines
could
be resolved by establishment of good eating patterns' intake
of
nutritionally balanced diet' appropriate nutrient supplementation
of
vitamins as well as minerals' and good nutrition program coupled
with a
regular exercise as mentioned in each chapters. Here is a Short
Summary
from the nutritional point of view for a longer' healthier' and
more
vital life. The balanced diet; especially the diet enhanced by
vitamins
E and B6 and trace mineral zinc is helpful for the elderly to
prevent
the declines in the immune system. The foods rich in vitamin
D and
calcium; they may help to prevent the elderly from osteoporosis.
The
foods with low fat' dietary cholesterol and sodium; these foods
may be
recommended for not only the elderly but also younger people
to reduce
the risk of cardiovascular disease. The good quality of diet;
it is
important for the elderly to avoid the monotonous diet because
of their
appetite declines.
Title
Nutrition and immunity with emphasis on infection and autoimmune
disease.
Author
Harbige LS
Address
Division of Immunology' United Medical School of Guy`s and St.
Thomas`s
Hospital' Rayne Institute' London' UK. 1.harbige@umds.ac.uk
Source
Nutr Health, 10(4):285-312 1996
Abstract
Nutrition and nutritional status can have profound effects on
immune
functions' resistance to infection and autoimmunity in man and
other
animals. Nutrients enhance or depress immune function depending
on the
nutrient and level of its intake. Protein-energy malnutrition
and
vitamin A deficiency are strongly associated with impaired immunity
and
infectious disease. The essential role vitamin A plays in infection
and
maintenance of mucosal surfaces has long been known. Recent evidence
shows that T-cell subpopulations' cytokines and antibody subclasses
are
all affected by vitamin A. In animal studies supplementation
with
vitamin E protects against infection and is linked to stimulatory
effects on the immune system. In man vitamin E and other anti-oxidants
increase the number of CD4+ cells. Dietary lipids and zinc have
a
substantial impact on autoimmunity from protective to potentiation
of
immuno-pathological processes in animals. There is considerable
potential to modify human autoimmune disease by manipulation
of lipid
nutrition. Deficiency of pyridoxine induces atrophy of lymphoid
organs'
marked reduction in lymphocyte numbers' impairs antibody responses
and
IL-2 production. Dietary copper is important in the prevention
of
infection in some animal species and T-cell function is defective
under
deficiency states due to an inability to produce IL-2. Selenium
has
been linked to viral infection' enhanced T-cell functions and
TNF beta
induced increase in natural killer cell activity. Understanding
the
molecular and cellular immunological mechanisms involved in
nutrient-immune interactions will increase our applications for
nutrition of the immune system in health and in disease
Title
zinc: an overview.
Author
Prasad AS
Address
Department of Internal Medicine' Wayne State University School
of
Medicine' Harper Hospital' Detroit' Michigan' USA.
Source
Nutrition, 11(1 Suppl):93-9 1995 Jan-Feb
Abstract
Zn deficiency in humans is widespread throughout the world. It
is more
prevalent in areas where the population subsists on cereal proteins.
Conditioned Zn deficiency is seen in many disease states. Its
deficiency during growth periods results in growth failure and
lack of
gonadal development in males. Other effects of Zn deficiency
include
skin changes' poor appetite' mental lethargy' delayed wound healing'
neurosensory disorders' and cell-mediated immune disorders. Severe
Zn
deficiency' as seen in acrodermatitis enteropathica (a genetic
disorder)' is fatal if Zn is not administered to these patients.
A
clinical diagnosis of marginal Zn deficiency in humans remains
problematic. Assays of Zn in granulocytes and lymphocytes provide
better diagnostic criteria for marginal Zn deficiency than plasma
Zn.
Approximately 300 enzymes are known to require Zn for their activities.
Zn is required for DNA synthesis' cell division' and protein
synthesis.
Recently' we learned that Zn-finger proteins are involved in
genetic
expression of various growth factors and steroid receptors. We
suspect
that several hundred Zn-containing nucleoproteins are probably
involved
in gene expression of various proteins. Zn deficiency adversely
affects
lymphocyte proliferation. This may be related to the enzymatic
role of
Zn in DNA synthesis and cell division. Thymulin' a thymic hormone
involved in T-lymphocyte maturation' is known to be Zn dependent
and is
adversely affected by Zn deficiency. Thus' an adverse effect
of Zn
deficiency may also be in lymphocyte differentiation and maturity.
Zn
deficiency is known to decrease interleukin 2 production by helper
T
lymphocytes' and abnormalities in T-lymphocyte subpopulations
have been
observed in Zn-deficient humans.(Abstract TRUNCATED AT 250 WORDS)
Title
Trace elements in biological samples and immunologic parameters
in
environmentally exposed populations (preliminary study)
Author
Boscolo P; Di Gioacchino M; Span`o A; Di Giacomo F; Ballone E;
D'Isidoro G; Cavallucci E; Giuliano G
Address
Centro di Medicina del Lavoro ed Ergoftalmologia, Dipartimento
di
Scienze, Statistica Medica, Universit`a G. D'Annunzio, Chieti.
Source
G Ital Med Lav Ergon, 19(1):53-5 1997 Jan-Mar
Abstract
In non-smoking policemen from a town of Central Italy, blood
CD4+
lymphocytes were reduced and CD8+ were increased as compared
with a
control group. This immunological alteration was not evident
in the
smoking policemen. Urine lead (marker of exposure to toxic agents
produced by traffic) and blood natural killer (NK) CD16+ lymphocytes
as
well as serum copper and HLA-DR+ cells (B, T, NK activated lymphocytes
and monocytes) were significantly correlated in the whole group
of 42
examined subjects. Another study was performed on 15 healthy
men,
occupationally not exposed to toxic agents and living in a suburban
area. Their urine lead, was positively correlated with the serum
IgA
immunoglobulins and negatively correlated with blood CD5(+)-CD19+
(a B
subset bearing the T CD5 antigen) lymphocytes. On the contrary,
urine
chromium was negatively correlated with serum IgA and positively
correlated with CD16(+)-56+ NK and CD5(+)-CD19+ B lymphocytes
as well
as with HLA-DR+cells. Serum zinc was also correlated with total
HLA-DR+and CD3-HLA+DR+ (activated B and NK lymphocytes and monocytes)
cells. These later data suggest that only zinc and copper but
also
trivalent chromium (to which normal population is mainly exposed
in
ordinary environmental conditions) may play a role in the mechanisms
regulating the immune response.
Title
Periplasmic copper-zinc superoxide dismutase protects Haemophilus
ducreyi from exogenous superoxide.
Author
San Mateo LR; Hobbs MM; Kawula TH
Address
Department of Microbiology and Immunology, University of North
Carolina
School of Medicine, Chapel Hill 27599, USA.
Source
Mol Microbiol, 27(2):391-404 1998 Jan
Abstract
Haemophilus ducreyi causes chancroid, a sexually transmitted
genital
ulcer disease implicated in increased heterosexual transmission
of HIV.
As part of an effort to identify H. ducreyi gene products involved
in
virulence and pathogenesis, we created random TnphoA insertion
mutations in an H. ducreyi 35000 library cloned in Escherichia
coli.
Inserts encoding exported or secreted PhoA fusion proteins were
characterized by DNA sequencing. One such clone encoded a Cu-Zn
superoxide dismutase (SOD) enzyme. The Cu-Zn SOD was periplasmic
in H.
ducreyi and accounted for most of the detectable SOD activity
in
whole-cell lysates of H. ducreyi grown in vitro. To investigate
the
function of the Cu-Zn SOD, we created a Cu-Zn SOD-deficient H.
ducreyi
strain by inserting a cat cassette into the sodC gene. The wild-type
and Cu-Zn SOD null mutant strains were equally resistant to excess
cytoplasmic superoxide induced by paraquat, demonstrating that
the
Cu-Zn SOD did not function in the detoxification of cytoplasmic
superoxide. However, the Cu-Zn SOD null strain was significantly
more
susceptible to killing by extracellular superoxide than the wild
type.
This result suggests that the H. ducreyi Cu-Zn SOD may play a
role in
bacterial defence against oxidative killing by host immune cells
during
infection.
Title
Laboratory markers as an index of aging.
Author
Narayanan S
Address
Department of Pathology' New York Medical College' Metropolitan
Hospital Center' New York' NY 10029.
Source
Ann Clin Lab Sci, 26(1):50-9 1996 Jan-Feb
Abstract
At the cellular level' mutations in deoxyribonucleic acid (DNA)
can
lead to synthesis of altered proteins which are unable to sustain
specific cell functions' eventually leading to its death. Veritably
apoptosis' or programmed cell death' is a device to eliminate
heavily
mutated cells. Cell membranes with altered proteins can be recognized
as foreign by the immune system' thus triggering autoimmunity.
Molecular biology techniques allow us to examine changes that
occur in
DNA' reflected by polymorphisms and variable numbers of tandem
repeats
(VNTR). A general decline in organ function is associated with
aging.
However' these changes may also be precipitated by disease processes.
Homeostatic control by the hypothalamus-pituitary-adrenal axis
is also
compromised with aging' leading to an increase in plasma
adrenocorticotrophic hormone (ACTH) and corticosteroid levels.
Derangement of the immune system with aging results in dysregulation
of
cytokine production. The ability of the cell to survive the onslaught
of oxygen-free radicals with enzymatic and nonenzymatic antioxidants'
and to repair DNA by activation of nuclear enzymes such as poly
(ADP-ribose) polymerase (PAD-PRP)' are some of determinants of
aging.
Title
Neutropenia caused by copper deficiency: possible mechanisms
of action.
Author
Percival SS
Address
Department of Food Science and Human Nutrition' University of
Florida'
Gainesville 32611' USA.
Source
Nutr Rev, 53(3):59-66 1995 Mar
Abstract
Although copper is an essential nutrient in the human diet' overt
or
severe copper deficiency is not a maJor public health concern
in the
United States. A marginal or borderline deficiency has been suggested
by researchers' although the widespread nature of copper deficiency
has
yet to be established. Reports indicate that copper deficiency
occurs
secondary to gastric resection' unsupplemented total parenteral
nutrition' high levels of zinc intake' or general malnutrition.
An
early clinical sign of copper deficiency is a reduction in the
number
of circulating neutrophils. Although copper is known to play
a wide
variety of roles in the organism and in the immune system' the
molecular mechanism for copper-deficient neutropenia is not known.
Very
little data exist with which to examine this question. This paper
will
summarize our existing knowledge of the mechanism by which copper
deficiency results in neutropenia. Although the data are scarce'
analysis of this question will allow us to better understand
additional
molecular roles of this trace element' and' in turn' to promote
an
improved knowledge of immune cell functions and cellular
differentiation.
Title
Nutritional implications in vascular endothelial cell metabolism.
Author
Hennig B; Toborek M; McClain CJ; Diana JN
Address
Department of Nutrition' University of Kentucky 40506-0054' USA.
Source
J Am Coll Nutr, 15(4):345-58 1996 Aug
Abstract
Endothelial cells interact with blood components and the abluminal
tissues' thus playing an active role in many aspects of vascular
function. Numerous physiologic and pathophysiologic stimuli are
often
mediated by nutrients that can contribute to the overall functions
of
endothelial cells in the regulation of vascular tone' coagulation'
cellular growth' immune and inflammatory responses. Therefore'
nutrient-mediated functional changes of the endothelium and the
underlying tissues may be significantly involved in disease processes
such as atherosclerosis. There is evidence that individual nutrients
or
nutrient derivatives may either provoke or prevent metabolic
and
physiologic perturbations of the vascular endothelium. Diets
high in
fat and/or calories are considered a risk factor for the development
of
atherosclerosis. Our research has shown that certain diet-derived
lipids and their derivatives can disrupt normal endothelial integrity'
thus reducing the ability of the endothelium to act as a selectively
permeable barrier to blood components. Mechanisms underlying
fatty
acid-mediated endothelial cell dysfunction may be related to
changes in
fatty acid composition as well as to an increase in cellular
oxidative
stress. Selective lipid accumulation and fatty acid changes in
endothelial cells can modulate membrane fluidity' proteoglycan
metabolism and signal transduction mechanisms. Most importantly'
dietary fats rich in certain unsaturated fatty acids' may be
atherogenic by enhancing the formation of reactive oxygen
intermediates. A subsequent imbalance in cellular oxidative
stress/antioxidant status can activate oxidative stress-responsive
transcription factors' which in turn may promote cytokine production'
expression of adhesion molecules on the surface of endothelial
cells'
and thus intensify an inflammatory response in atherosclerosis.
Our
data also suggest that certain nutrients' which have antioxidant
and/or
membrane stabilizing properties' can protect endothelial cells
by
interfering with lipid/cytokine-mediated endothelial cell dysfunction.
These findings contribute to the understanding of the interactive
role
of dietary fats with inflammatory components' as well as with
nutrients
that exhibit antiatherogenic properties' in the development of
atherosclerosis. |
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