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EDTA doesnot enter cells, because it cannot cross cell membranes.

EDTA has the capacity to chelate almostevery positive ion in the periodic table.

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But EDTA chelation of calcium has the capacity to kill cells.

By the early 1980s, basing theory on more recent knowledgeof free-radical effects on tissue, proponents posited a new andcurrent theory of free-radical neutralization. The proposed mechanismwas that toxic metals such as iron and copper, released by clotlysis at arterial injury sites, generate free radicals that oxidizefatty acids to lipid peroxides, which then would generate newfree radicals. This chain of oxidation reactions would cause arterialcell membrane damage and plaque formation. This mechanism wasmore in line with then-current thinking on the pathophysiologyof atherosclerosis. Advocates then claimed that through EDTA binding,iron would become chemically nonreactive, cease catalyzing free-radicalproduction, and thus curb the pathological processes that causeatheromas [4].

Intravenous EDTA Chelation Therapy   Click Here to Change Font Size

N Z Med J 101:109, 1988.

Sehnert KW, Claque AF, and Cheraskin E: The improvement in renal function following EDTA chelation and multivitamin trace mineral therapy: A study in creatinine clearance.

You have been redirected from EDTA iron(III) sodium salt trihydrate

≥98 %, for synthesisEDTA iron(III) sodium salt trihydrate, Iron(III) EDTA sodium salt trihydrate

Ann Intern Med 70:1007, 1969.

Fuleihan FJD, Kurban AK, Abboud RT, Beidas-jubran N and Farah FS: An objective evaluation of the treatment of systemic scleroderma with disodium EDTA, pyridoxine and reserpine.

Aust Ann Med 12:310, 1963.

Estep HL, Gardner CT Jr, Taylor JP, Minott A and Tucker HStG Jr: Phosphate excretion patterns following intravenous injection of ethylenediaminetetraacetate ((EDTA).

An ADI of 2.5 mg EDTA CaNa2EDTA/kg body weight/day was established.

EDTA   Ethyldiaminetetraacetic acid, also known as EDTA is used to chelate metal ions.

The available studies indicated that only a fraction, if any, of the iron EDTA chelate is absorbed as such, that EDTA from sodium iron EDTA is only poorly absorbed and that the majority is excreted in the faeces.

The Committee noted that sodium iron EDTA dissociates in the intestine, and iron in this form is approximately twice as bioavailable as iron in the form of iron sulfate.

This monograph discusses the safety of NaFeEDTA for food fortification in developing countries.
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  • Over time EDTA can disserve its function.

    preparation is under stirring, but precipitation occurs if the iron compound is added to the EDTA!!!!!!!

  • of the zinc or liver is freely available to EDTA.

    Cobalt EDTA

  • EDTA removes about 1.4 per cent.

    Sodium iron EDTA has not previously been evaluated by the Joint FAO/WHO Expert Committee on Food Additives.

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of 6 mg/kg body-weight oral FeEDTA but only 25 per cent.

The chelate holds the iron in solution as the pH rises in the upper small intestine, but the strength of the complex is progressively reduced allowing at least partial exchange with other metals and the release of some of the iron for absorption.

Na59FeEDTA was administered to human volunteers.

There is convincing evidence that iron chelated by EDTA (NaFeEDTA) is available for absorption via the physiologically regulated pathways responsible for iron uptake (Candela et al., 1984).

EDTA is a synthetic amino acid.

The maximum radioactivity in the urine after application of 14C-labelled CaNa2EDTA to the skin was only 10 ppm (Foreman & Trujillo, 1954).

One thing is for sure, EDTA is not biodegradable!

2.1.1 Absorption and excretion Absorption and excretion of Fe from NaFeEDTA - Injection studies When NaFeEDTA is injected intravenously into rats most of the iron (70-90%) is lost through the urine within 24 hours (Najarajan et al., 1964; Anghileri, 1967).

Iron chelates consist of three components:

was almost quantitatively excreted in the urine, it was concluded that FeEDTA was degraded prior to absorption, when given orally (Lapinleimu & Wegelius, 1959).

It has been shown conclusively: EDTA restores this lost blood flow.

The longer contact time between transferrin and EDTA, allows for greater transfer of iron from the chelate to the physiological transport protein (Rubin et al., 1970).

How can this happen, if EDTA is not a "ROTO-ROOTER"?

The synthesis of the ligand is described: the acid dissociation constants and the stability constants of its iron (III) complex were determined potentiometrically and through spectrophotometric competition with EDTA.

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