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Detox and Chelation
Magnesium – Antioxidant Status – Glutathione
The involvement of free radicals in tissue
injury induced by Mg deficiency[i] causes an accumulation of
oxidative products in heart, liver, kidney, skeletal muscle
tissues and in red blood cells.[ii] Magnesium is a crucial
factor in the natural self-cleansing and detoxification
responses of the body. It stimulates the sodium potassium pump
on the cell wall and this initiates the cleansing process in
part because the sodium-potassium-ATPase pump regulates
intracellular and extracellular potassium levels. Cell membranes
contain a sodium/potassium ATPase, a protein that uses the
energy of ATP to pump sodium ions out of the cell, and potassium
ions into the cell. The pump works all of the time, like a bilge
pump in a leaky boat, pumping K+ and Na+ in and out,
respectively.
Potassium regulation is of course crucial because potassium acts
as a counter flow for sodium's role in nerve transmission. The
body must put a high priority on regulating the potassium of the
blood serum and this becomes difficult when magnesium levels
become deficient.[iii] Because of these crucial relationships,
when magnesium levels become dramatically deficient we see
symptoms such as convulsions, gross muscular tremor, atheloid
movements, muscular weakness, virtigo, auditory hyperacusis,
aggressiveness, excessive irritability, hallucinations,
confusion, and semicomma. A magnesium deficiency can cause the
body to lose potassium and this our bodies cannot afford. Within
the cell wall is a sodium pump to provide a high internal
potassium and a low internal sodium. Magnesium and potassium
inside the cell assist oxidation, and sodium and calcium outside
the cell wall help transmit the energy produced. The healthy
cell wall favors intake of nutrients and elimination of waste
products.
Magnesium protects cells from aluminum, mercury, lead, cadmium,
beryllium and nickel, which explains why re-mineralization is so
essential for heavy metal detoxification and chelation.
Magnesium protects the cell against oxyradical damage and
assists in the absorption and metabolism of B vitamins, vitamin
C and E, which are anti-oxidants important in cell protection.
Recent evidence suggests that vitamin E enhances glutathione
levels and may play a protective role in magnesium
deficiency-induced cardiac lesions.[iv] Magnesium in general is
essential for the survival of our cells but takes on further
importance in the age of toxicity where our bodies are being
bombarded on a daily basis with heavy metals. Magnesium thus
protects the brain from toxic effects of chemicals. It is highly
likely that low total body magnesium contributes to heavy metal
toxicity in children and is a strong participant in the etiology
of learning disorders.
Without sufficient magnesium, the body accumulates toxins and
acid residues, degenerates rapidly, and ages prematurely. Recent
research has pointed to low glutathione levels being responsible
for children’s vulnerability to mercury poisoning from vaccines.[v]
It seems more than reasonable to assume that low levels of
magnesium would also render a child vulnerable. And in fact we
find out that glutathione requires magnesium for its synthesis.[vi]
Glutathione synthetase requires γ-glutamyl cysteine, glycine,
ATP, and magnesium ions to form glutathione.[vii] In
magnesium deficiency, the enzyme y-glutamyl transpeptidase is
lowered.[viii] Data demonstrates a direct action of glutathione
both in vivo and in vitro to enhance intracellular magnesium and
a clinical linkage between cellular magnesium, GSH/GSSG ratios,
and tissue glucose metabolism.[ix] Magnesium deficiency causes
glutathione loss, which is not affordable because glutathione
helps to defend the body against damage from cigarette smoking,
exposure to radiation, cancer chemotherapy, and toxins such as
alcohol and just about everything else.
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[i] Magnesium deficiency (MgD) has been associated with
production of reactive oxygen species, cytokines, and
eicosanoids, as well as vascular compromise in vivo. Although
MgD-induced inflammatory change occurs during "chronic" MgD in
vivo, acute MgD may also affect the vasculature and consequently,
predispose endothelial cells (EC) to perturbations associated
with chronic MgD. As oxyradical production is a significant
component of chronic MgD, we examined the effect of acute MgD on
EC oxidant production in vitro. In addition we determined EC;
pH, mitochondrial function, lysosomal integrity and general
cellular antioxidant capacity. Decreasing Mg2+ (< or =
250microM) significantlyincreased EC oxidant production relative
to control Mg2+ (1000microM). MgD-induced oxidant production,
occurring within 30min, was attenuated by EC treatment with
oxyradical scavengers and inhibitors of eicosanoid biosynthesis.
Coincident with increased oxidant production were reductions in
intracellular glutathione (GSH) and corresponding EC
alkalinization. These data suggest that acute MgD is sufficient
for induction of EC oxidant production, the extent of which may
determine, at least in part, the extent of EC dysfunction/injury
associated with chronic MgD. Effect of acute magnesium
deficiency (MgD) on aortic endothelial cell (EC) oxidant
production.Wiles ME, Wagner TL, Weglicki WB.The George
Washington University Medical Center, Division of Experimental
Medicine, Washington, D.C., USA.
mwiles@nexstar.com
Life Sci. 1997;60(3):221-36.
[ii] Martin, Hélène. Richert, Lysiane. Berthelot, Alain
Magnesium Deficiency Induces Apoptosis in Primary Cultures of
Rat Hepatocytes.* Laboratoire de Physiologie, et Laboratoire de
Biologie Cellulaire, UFR des Sciences Médicales et
Pharmaceutiques, Besançon, France. 2003 The American Society for
Nutritional Sciences J. Nutr. 133:2505-2511, August 2003
[iii] A magnesium deficiency can cause the body to lose
potassium [Peterson 1963][MacIntyre][Manitius], possibly because
of a poorly understood effect of magnesium on the efficiency of
energy supply to the sodium pump [Fischer].
[iv] Barbagallo, Mario et al. Effects of Vitamin E and
Glutathione on Glucose Metabolism: Role of Magnesium; (Hypertension.
1999;34:1002-1006.)
[v] Enviroonmental Working Group.
http://www.ewg.org/reports/autism/part1.php
[vi] Linus Pauling Institute
http://lpi.oregonstate.edu/infocenter/minerals/magnesium/index.html#function
[vii] Virginia Minnich, M. B. Smith, M. J. Brauner, and Philip
W. Majerus. Glutathione biosynthesis in human erythrocytes.
Department of Internal Medicine, Washington University School of
Medicine, J Clin Invest. 1971 March; 50(3): 507–513. Abstract:
The two enzymes required for de novo glutathione synthesis,
glutamyl cysteine synthetase and glutathione synthetase, have
been demonstrated in hemolysates of human erythrocytes. Glutamyl
cysteine synthetase requires glutamic acid, cysteine, adenosine
triphosphate (ATP), and magnesium ions to form γ-glutamyl
cysteine. The activity of this enzyme in hemolysates from 25
normal subjects was 0.43±0.04 μmole glutamyl cysteine formed per
g hemoglobin per min. Glutathione synthetase requires γ-glutamyl
cysteine, glycine, ATP, and magnesium ions to form glutathione.
The activity of this enzyme in hemolysates from 25 normal
subjects was 0.19±0.03 μmole glutathione formed per g hemoglobin
per min. Glutathione synthetase also catalyzes an exchange
reaction between glycine and glutathione, but this reaction is
not significant under the conditions used for assay of
hemolysates. The capacity for erythrocytes to synthesize
glutathione exceeds the rate of glutathione turnover by 150-fold,
indicating that there is considerable reserve capacity for
glutathione synthesis. A patient with erythrocyte glutathione
synthetase deficiency has been described. The inability of
patients' extracts to synthesize glutathione is corrected by the
addition of pure glutathione synthetase, indicating that there
is no inhibitor in the patients' erythrocytes.
[viii] Braverman, E.R. (with Pfeiffer, C.C.)(1987). The healing
nutrients within: Facts, findings and new research on amino
acids. New Canaan: Keats Publishing.
[ix] Barbagallo, M. et al. Effects of glutathione on red blood
cell intracellular magnesium: relation to glucose metabolism.
Hypertension. 1999 Jul;34(1):76-82. Institute of Internal
Medicine and Geriatrics, University of Palermo, Italy.
mabar@unipa.it
More on this subject is available in the book
Transdermal Magnesium Therapy.
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