Ethylenediaminetetraacetic Acid (EDTA)

Ethylenediaminetetraacetic acid induces antioxidant and anti-inflammatory activities in experimental liver fibrosis.
González-Cuevas J, Navarro-Partida J, Marquez-Aguirre AL, Bueno-Topete MR, Beas-Zarate C, Armendáriz-Borunda J.
Redox Rep. 2011;16(2):62-70.

 Experimental liver fibrosis induced by carbon tetrachloride (CCl(4)) is associated with oxidative stress, lipid peroxidation, and inflammation. This work was focused on elucidating the anti-inflammatory and antioxidant effects of ethylenediaminetetraacetic acid (EDTA) in this model of hepatotoxicity Methods: Wistar male rats were treated with CCl(4) and EDTA (60, 120, or 240 mg/kg). Morphometric analyses were carried out in Masson’s stained liver sections to determine fibrosis index. Coagulation tests prothrombin time (PT) and partial thromboplastin time (PTT) were also determined. Gene expression for transforming growth factor beta (TGF-beta1), alpha1(I) procollagen gene (alpha1 Col I), tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6), and superoxide dismutase (SOD) was monitored by real-time PCR. Antioxidant effect of EDTA was measured by its effects on lipid peroxidation; biological activity of ceruloplasmin (Cp), SOD, and catalase (Cat) were analyzed by zymography assays. Animals with CCl(4)-hepatic injury that received EDTA showed a decrement in fibrosis (20%) and lipid peroxidation (22%). The mRNA expression for TNF-alpha (55%), TGF-beta1 (50%), IL-6 (52%), and alpha1 Col I (60%) was also decreased. This group of animals showed increased Cp (62%) and SOD (25%) biological activities. Coagulation blood tests, Cat activity, and gene expression for SOD were not modified by EDTA treatment. This study demonstrates that EDTA treatment induces the activity of antioxidant enzymes, decreases lipid peroxidation, hepatic inflammation, and fibrosis in experimental liver fibrosis induced by CCl(4). PMID: 21722414
 

A pilot double-blind study of sodium-magnesium EDTA in peripheral vascular disease.
Olszewer E, Sabbag FC, Carter JP.
J Natl Med Assoc. 1990 Mar;82(3):173-7.

 Ten male patients with peripheral vascular disease, Type 2 (LaFontaine), were randomly assigned in a double-blind study to receive either Na2 ethylene diamine tetra acetic acid (EDTA) plus MgSO4, B complex, and vitamin C, or a placebo of MgSO4, B complex, and vitamin C in Ringer’s lactate solution. A total of 20 intravenous infusions were planned for administration to each patient. Clinical and laboratory (noninvasive) tests showed dramatic improvements after 10 infusions in some patients, and thus was broken the code indicating who was receiving EDTA and who was receiving placebo. The group that improved had been receiving EDTA; there was no change in the placebo group. The trial was then completed in a single-blind fashion. Patients originally assigned to receive placebo then received 10 EDTA infusions, while the group originally assigned to EDTA received 20 EDTA infusions. The group that had formerly received placebo showed improvements comparable to those seen in the first EDTA group after 10 treatments. PMID: 2108254

  Role of EDTA chelation therapy in cardiovascular diseases.
Shrihari JS, Roy A, Prabhakaran D, Reddy KS.
Natl Med J India. 2006 Jan-Feb;19(1):24-6.

 Chelation therapy is a widely practised mode of treatment for atherosclerotic cardiovascular diseases all over the world. However, evidence for the utility of this therapy is limited and conflicting. We did a systematic review of the literature. The reference listings of the articles, obtained from a Pubmed search using relevant keywords, were searched for additional related articles. Most of the evidence supporting the use of EDTA chelation therapy is from case reports, small series or uncontrolled, open-label clinical trials. The published randomized controlled trials include few patients and their results are of limited value. Uncontrolled studies have reported symptomatic improvements but the few controlled trials suggest that these benefits are due to a placebo effect. The available data do not support the use of chelation in cardiovascular diseases. This therapy should be used only in the context of a research trial including patients who have failed to respond to conventional treatment. PMID: 16570682