Rooney, 2007. Mercury and DMPS, DMSA, ALA, NAC, GSH, selenium, zinc, fiber

[Guest guest]

Rooney has written an excellent -- and very readable -- review of chronic, low-dose mercury exposure. Anyone interested in mercury should read this article.

It discusses the different forms of mercury, half-life and excretion, mercury transport in the body, DMSA, DMPS, ALA, NAC, GSH, zinc, selenium, and dietary fiber. He even discusses the interactions of these -- e.g., what happens if you take DMSA and selenium at the same time (not recommended). NAC and GSH may also be counterproductive. And he even considers dosing protocols and gives favorable mention to Cutler.

He reviews the common urine and blood diagnostic test, including challenge tests, and why they don't work and cause complications.

I assume that you all know that Abraham has reported increased levels of mercury (and other metals) excretion in urine in those supplementing with Iodoral. Unfortunately, he has not yet published the data. And HOW iodine may be interacting with mercury is not yet known.

http://iodine4health.com/special/metals/abraham_metals.htm

Zoe

The role of thiols, dithiols, nutritional factors and interacting ligands in the toxicology of mercury.

Rooney JP.Toxicology. 2007 Mar 1; [Epub ahead of print]

"Mercury has been a known as a toxic substance for centuries. Whilst the clinical features of acute mercury poisoning have been well described, chronic low dose exposure to mercury remains poorly characterised and its potential role in various chronic disease states remains controversial. Low molecular weight thiols, i.e. sulfhydryl containing molecules such as cysteine, are emerging as important factors in the transport and distribution of mercury throughout the body due to the phenomenon of "Molecular Mimicry" and its role in the molecular transport of mercury. Chelation agents such as the dithiols sodium 2,3-dimercaptopropanesulfate (DMPS) and meso-2,3-dimercaptosuccinic acid (DMSA) are the treatments of choice for mercury toxicity. Alpha-lipoic acid (ALA), a disulfide, and its metabolite dihydrolipoic acid (DHLA), a dithiol, have also been shown to have chelation properties when used in an appropriate manner. Whilst N-acetyl-cysteine (NAC) and glutathione (GSH) have been recommended in the treatment of mercury toxicity in the past, an examination of available evidence suggests these agents may in fact be counterproductive. Zinc and selenium have also been shown to exert protective effects against mercury toxicity, most likely mediated by induction of the metal binding proteins metallothionein and selenoprotein-P. Evidence suggests however that the co-administration of selenium and dithiol chelation agents during treatment may also be counter-productive. Finally, the issue of diagnostic testing for chronic, historical or low dose mercury poisoning is considered including an analysis of the influence of ligand interactions and nutritional factors upon the accuracy of "chelation challenge" tests."

http://iodine4health.com/special/metals/rooney_metals.htm

"This review specifically focuses on the influence of thiols, dithiols and interacting ligands such as zinc and selenium containing proteins on the toxicity of mercury at the molecular level (see Table 1 for summary). It also assesses the implications of these molecules on the clinical testing of mercury toxicity, considered within the context of chronic long-term sub-clinical exposure to the different forms of mercury with the likely selective retention by the brain of inorganic mercury over time."

"Chelators are molecules that tightly bind in a ring structure to metals. A good clinical chelator will have low toxicity, will preferentially bind to the heavy metal with a high stability constant and will have a higher excretion rate than endogenous binding species for the metal, thus favouring fast elimination of the toxic metal. DMPS and DMSA are dithiol chelating agents used in the treatment of mercury toxicity."

"Frequent treatments with lower doses of ALA could also be effective by virtue of keeping the blood level of ALA more constant, and this has been observed in guinea pigs.... ALA administered alone or with DMSA did not chelate mercury in kidney or brain when administered to rats exposed to repeated doses of mercury vapour.... However, ... administration of ALA to rats led to a greatly increased biliary excretion of inorganic mercury (12- to 37-fold).... Further research is needed into the actions of ALA as a chelator--in particular investigation of frequent low dose chelation as suggested by Cutler (1999).... The effect of ALA on mercury toxicity is dependent on dosage size and on the spacing of dosages in time."

"In humans, control of plasma cysteine levels is important in the control of symptoms and the treatment of mercury toxicity."

"Given the inefficiency of elimination of methylmercury via the bile, the known entero-hepatic cycling of methylmercury and the mercury uptake mechanisms of the kidneys and the brain..., NAC and GSH would appear to be poor treatment choices for mercury toxicity due to the high risk of redistribution of mercury to those organs."

"Selenium in plasma forms a complex with inorganic mercury, which then binds to selenoprotein-P..., which in turn seems to prevent mercury uptake by the kidneys."

"Observed in rats that simultaneous administration of selenium (in the form of sodium selenite) and a chelating agent (DMSA or DMPS) leads to reduced excretion and considerable redistribution of mercury -- specifically a reduction of kidney mercury and an increase in liver concentrations although it should be noted other organs were not examined in this study."

"Since the chelators used (DMSA and DMPS) act to increase urinary excretion of mercury and since selenoprotein-P seems to prevent uptake of mercury by the kidneys, Juresa et al (2005) proposed that ligand competition between the chelators and selenoprotein-P led to the redistribution of mercury and decreased urinary excretion."

"Increased dietary fibre may increase the elimination of methylmercury...."

"It is likely that thiol, selenium and possibly zinc levels have an effect (directly or indirectly) on the distribution of mercury. Little is known about the interaction of these species with the chelating drugs DMSA or DMPS, although it has been seen that simultaneous administration of selenium with DMSA or DMPS leads to reduced effectiveness of the chelators."

"DMPS and DMSA are the drugs of choice in the treatment of mercury poisoning.... They are ineffective at chelating mercury from the brain."

"Currently, ALA represents the only potential chelating agent capable of accessing the central and peripheral nervous system.... Its actions are dependent on both dose size and timing."