Detox and Chelation

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Detox and Chelation

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Magnesium – Antioxidant Status – Glutathione

 

The involvement of free radicals in tissue injury induced by Mg deficiency

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.

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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  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