heavy metal detox

Other Detox methods

Dan Purser GSH

This post is a mixture of “other” heavy metal deox methods

Dr Purser has an interesting claim that GSH is stuck to the surface of immune cells so that it can bind heavy metals. He did not say if GSH was covalent bound by the thiol of cysteine, a carboxyl of glutamate or glycine. Images from the video are shown so that the reader may browse the video to listen more carefully to the content.

He mentioned metallothionein that should be antiviral. HIV. Metalothonine requires reduced GSH. Should help with burns…GSH should help with neuropathy and neuropathic pain… CD4 CD8 T cells… GSH is removing inflammatory substances. Should help with mental clarity, should help with kidney disease, growth of new nephrons… This video has a brain storming, whirlwind presentation of ideas feel to it.

This compound may have been in the pipeline at the time of the video. There was mention of a GSH and metallothionein connection that deserves an image.

This study was a collaboration between scientists in Saudia Arabia and Egypt. On the surface it was not evident why they thought to connect Hg generation of reactive oxygen species and melatonin. “The cytoplasmic enzyme quinone reductase 2 (QR2), designated as receptor MT3, has a detoxifying activity reducing melatonin oxidative damage” The Wikipedia page on NAD(P)H dehydrogenase, quinone 2, NQO2, gives us reason to entertain a study that, on the surface, appears to engage sloppy thinking. Not only does NQO2 bind melatonin, it also has two Zn2+ binding sites that do not appear to be catalytic. Hg2+ and Zn2+ are in the same Periodic Table of Elements group.

This image was adapted from the UniProt.org NQO2 entry. Additional information includes : The enzyme apparently serves as a quinone reductase in connection with conjugation reactions of hydroquinones involved in detoxification pathways as well as in biosynthetic processes such as the vitamin K-dependent gamma-carboxylation of glutamate residues in prothrombin synthesis.Uses dihydronicotinamide riboside (NRH) rather than NAD(P)H as an electron donor.

Just browsing PubMed titles, melatonin is an inhibitor of NQO2. The Saudi/Egyptian groups dosed male rats with high and low amounts of HgCl2 with and without melatonin from a U.S. supplier.

Effect of melatonin on SOD (A), catalase (B) and GSP (C) in brain tissue of mercuric chloride-induced neurotoxicity in rats. Values are expressed as mean ± SD, (n = 6). # is significant compared to control group. $ significant compared to LD HgCl2 group. @ significant compared to HD HgCl2 group. & significant compared to LD HgCl2+MLT group. Significant (p < 0.05). [2]

There was more to this study than is being presented in this post. The authors totally dropped the NQO2 “melatonin receptor” from their discussion. They speculated on new gene transcripts without actually measuring protein and/or mRNA levels. They were just measuring enzyme activities. Meltatonin seems to be doing something.

Zinc Detox and exocytosis [3,4]

This post is going to totally skip the experiments that established the following model of Zn2+ inducing the expression of lysosomeal Zn2+ transporters. [4] UniProt does not have a lot to say about Slc30A1 the Zn2+/H+ lysosomal anti-porter that might also pump Zn2+ into lysosomal membranes, particularly of macrophage.

A model of lysosomal Zn2+ sink and its role in Zn2+ detoxification. (A) Under normal conditions, Zn2+ enters the cells through ion channels and ZIPs and is (1) recognized by the Zn2+-sensitive transcription factor MTF-1 that, once Zn2+-bound, translocates to the nucleus to upregulate ZnT1 and MT2a gene expression. (2) Zn2+ is transported out of the cytoplasm and into the lysosome through ZnT2 and ZnT4. Zn2+ that builds up in the lysosomal Zn2+ sink is then secreted across the plasma membrane (3) through a VAMP7-dependent mechanism. This prevents toxic Zn2+ buildup in the cytoplasm and other organelles (4). A piece of the periodic table of elements with a focus on metals has been added. Note that lead, Pb, is in the same group as carbon and silicon.

A PubMed search on ZnT1 + cadmium reveals that Zn2+ and Cd2+ can induce the expression of ZnT1 as well as be transported by this protein. A similar search for mercury and ZnT1 did not reveal evidence of molecular mimicry. Reference [4] offers a nice overview of lysosomal pathways for further reading.


Copper Balance [5]

“Copper Balance is a supplement blend of zinc, molybdenum, boron, and B6 to turn dysfunctional metallothioneins into functional proteins. Now these fully functional metallothioneins are equipped to break down and collect the copper that has built up around the body. Drastic improvements can be felt rapidly, but again, things can take time.” The intent is to treat pain associated with fibromyalgia.

The ingredient list is for the Copper Balance supplement. Lidocaine is a local anesthetic that acts by inhibiting voltage gated sodium channels.

Excess zinc can sometimes lead to copper deficiency. The molybdemun seems to address the issue of molebdenum cofactor deficiency that has another “cure” with a patent. We will also be getting to the 10x excess of B6. [6]

  1. Mitochondrial inner membrane Sulfite oxidase (SOX) catalyzes the terminal step in oxidative cysteine catabolism, the oxidation of sulfite to sulfate. Sulfite oxidation to the reduction of cytochrome c.
  2. Cytosolic xanthine oxidoreductase and
  3. aldehyde oxidase are closely related Mo–iron–flavin enzymes catalyzing the hydroxylation reactions of purines and various heterocyclic substrates.
  4. Mitochondrial amidoxime-reducing component (mARC) has been identified as a fourth vertebrate Mo-enzyme and reduces N-hydroxylated prodrugs as well as metabolites such as N-hydroxy-L-arginine.

Some treatments of molybdenum cofactor deficiency include cyclic pyranopterin monophosphate, (cPMP) Pyridoxine is the 4-methanol form of vitamin B6 and is converted to pyridoxal 5-phosphate in the body. The first enzyme, SOX, is probably the only one we really need to worry about then dealing with supplementation with GSH and other thiol containing compounds like ALA that might need to be metabolized.

Do those that supplement with ALA suffer side effects because lack of Mo replete SOX results in H2S build up? The same might be said about N-acetyl cysteine supplementation, if this is true.

Sweating [7]

This study involved 12 university students in New Taipei Taiwan, six males and six females. [7[

Note that 10x as much lead and nickle are seated out by exercise than by sedentary heat.

In their discussion these authors claim that there are two sources of heavy metals in our bodies: our mothers and environmental exposure. The authors also claimed that most of the Hg in the blood is stored as Me-Hg in RBC. This just does not seem to jive the high thiol reactivity of Hg. The authors did not address the potential of large amounts of Cu in the sweat being due to ATP7B. The differences between static heat and exercise heat are most different for Ni and Pb.


  1. YouTube link, then selling his brand VARS
  2. Said ES, Ahmed RM, Mohammed RA, Morsi EM, Elmahdi MH, Elsayed HS, Mahmoud RH, Nadwa EH. Ameliorating effect of melatonin on mercuric chloride-induced neurotoxicity in rats. Heliyon. 2021 Jul 6;7(7):e07485 PMC free article
  3. Kukic I, Kelleher SL, Kiselyov K. Zn2+ efflux through lysosomal exocytosis prevents Zn2+-induced toxicity. J Cell Sci. 2014 Jul 15;127(Pt 14):3094-103. PMC free article
  4. Buratta S, Tancini B, Sagini K, Delo F, Chiaradia E, Urbanelli L, Emiliani C. Lysosomal Exocytosis, Exosome Release and Secretory Autophagy: The Autophagic- and Endo-Lysosomal Systems Go Extracellular. Int J Mol Sci. 2020 Apr 8;21(7):2576 PMC free article
  5. Dan Purser MD
  6. Johannes L, Fu CY, Schwarz G. Molybdenum Cofactor Deficiency in Humans. Molecules. 2022 Oct 14;27(20):6896. PMC free article
  7. Kuan WH, Chen YL, Liu CL. Excretion of Ni, Pb, Cu, As, and Hg in Sweat under Two Sweating Conditions. Int J Environ Res Public Health. 2022 Apr 4;19(7):4323 PMC free article

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