|
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 ?-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.
---------------------------------------------------------------------------
[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 ?-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 ?-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
IMVA - Article
- by Mark Sircus, Ac., OMD, author of Transdermal
Magnesium Therapy.
|
