Remove Toxic Metals With Chelation Therapy

  Contact : GET MORE INFO

The Metabolic Effects of Heavy Metals

heavymetaltoxinsdianaThe Metabolic Effects of Toxic Heavy Metals

The knowledge gained about the homeostasis of heavy metals has been substantial over more than a decade. Although they have no known metabolic function, when present in the body they disrupt normal cellular processes, leading to toxicity in a number of organs. They are relatively poorly absorbed into the body, but once absorbed are slowly excreted and accumulate in the body causing organ damage. Thus, their toxicity is in large part due to their accumulation in biological tissues, including food animals such as fish and cattle as well as humans. Distribution of heavy metals in the body relies on its binding to carrier molecules in the circulation. Metallothioneins are small proteins rich in cysteine residues, which accounts for the unique metal-binding properties of metallothioneins and play a major role in the dispersal and storage of heavy metals in the body. They also accumulate in hair and toenails (e.g., arsenic and mercury), which both can be used as indicators of long-term exposure in population studies. These heavy metals have a slow excretion rate from the body, as indicated by their long half-life time (e.g., half-life of lead is 27 year in cortical bone and 16 year in cancellous bone, half-life of cadmium is 10–30 years), compared with their uptake rate.


After ingesting inorganic arsenic compounds, the absorbed arsenic is metabolized primarily by the liver and excreted by the kidneys into the urine within a few days after exposure. Organic arsenic species in fish are also rapidly absorbed. In comparison to inorganic forms, organic compounds are much less extensively metabolized in the human body and more rapidly eliminated in urine with less than 5% was found to be eliminated in feces. In addition to gastrointestinal, dermal, or pulmonary uptake, exposure to organic arsenic species originates from methylation of inorganic arsenic inside the human body, which is regarded as a detoxification mechanism, since the methylated metabolites exert less acute toxicity and reactivity with tissue constituents than inorganic arsenic. The central site for arsenic methylation in the human body is the liver. These methylated metabolites can be eliminated in the bile. Factors such as dose, age, gender, and smoking contribute only minimally to the large interindividual variation in arsenic methylation observed in humans (reviewed by [53]).


The gastrointestinal absorption of lead is higher for children (30–50%) than for adults (5–10%). The absorbed lead is distributed to blood, soft tissue, and bone. In blood, red blood cells virtually bind all of the lead (9899%), thus only 12% of blood lead are present in plasma. Gastrointestinal absorption and retention, the major pathway of lead intake, have been shown to vary widely depending on the chemical environment of the gastrointestinal lumen, age, and iron stores (nutritional status of the subject). Certain dietary components may act by increasing lead solubility, such as ascorbic acid, amino acids, vitamin D, protein, fat, and lactose, thus enhancing its absorption. Total body content of lead does not have a feedback mechanism which limits its absorption. Absorbed lead is mainly excreted in urine, whereas the feces contain predominantly unabsorbed lead. Being one of the calcium-like elements, lead follows the movement of calcium in the body to a large extent, and physiologic regulators of calcium metabolism usually affect the behavior of lead in a similar manner. Although bone has been considered a storage site for more than 90% of the total body burden, increased bone turnover in times of physiological (e.g., pregnancy or lactation) and pathological (e.g., osteoporosis) conditions release lead from bone. Lead can be remobilized from bone by competing with calcium for transport and for binding sites and is released, along with calcium, when bone is resorbed (reviewed by [54]). The mechanisms by which both elements enter and leave the bone are similar and through these mechanisms, bone lead equilibrates with blood lead [55].


The possible range of intestinal absorption rate for cadmium was established to be between 3 and 7% in humans and was used to assign an average 5% absorption rate in deriving a safe exposure level [56]. However, higher cadmium absorption rates (20–40%) were observed among young subjects and considered biliary excretion and reuptake via enterohepatic circulation to be the most likely possible reason. The duodenal iron transporter is upregulated by iron deficiency, which leads to an increased intestinal absorption of dietary cadmium. This is probably the main reason why the body burden of cadmium is generally higher among women [57] whose prevalence of iron depletion is higher than that of men. Once absorbed, cadmium binds avidly to metallothionein. Cadmium irreversibly accumulates in the human body, particularly in kidneys and liver. Because there is no efficient excretory mechanism for cadmium from the body and it is bound with high affinity to metallothionein within cells. Accumulation of cadmium mainly in liver and kidney and also in testes is due to the ability of these tissues to synthesize metallothionein, a cadmium-inducible protein that protects the cell by tightly binding the toxic cadmium ion. The kidney is regarded as critical organ for its accumulation and toxicity. Greater than one-third of body cadmium deposits are found in the kidney, especially in subjects with low environmental exposure. By far, the most toxicological property of cadmium is its exceptionally long half-life in the human body and thus its low excretion rate (reviewed by [30]).


Dietary methylmercury is well absorbed from the gastrointestinal tract, readily enters the bloodstream, and is distributed to all tissues. About 5% of the body load is found in the blood compartment, and about 10% is found in the brain. 95% of the methylmercury in blood is bound to erythrocytes leaving 5% present in plasma. Less than 1% of the body burden of methylmercury is excreted per day, mainly via the feces. In the body, methylmercury is mainly, if not exclusively, bound to the sulfur atom of thiol ligands. Methylmercury is metabolized to inorganic mercury prior to elimination via feces, but the rate of conversion is slow (the half-life is about 70–80 days). In the liver and kidney, it is rapidly converted to inorganic mercury and stored as divalent mercury cation. This, together with the fact that the human body has no way of excreting mercury actively, means that mercury continues to accumulate in the body throughout life (reviewed by [31]).


30. T. S. Nawrot, J. A. Staessen, H. A. Roels et al., “Cadmium exposure in the population: from health risks to strategies of prevention,” BioMetals, vol. 23, no. 5, pp. 769–782, 2010. View at Publisher · View at Google Scholar · View at PubMed

31. S. Díez, “Human health effects of methylmercury exposure,” Reviews of Environmental Contamination and Toxicology, vol. 198, pp. 111–132, 2009. View at Google Scholar

53. E. Dopp, A. Kligerman, and R. Diaz-Bone, “Organoarsenicals. Uptake, metabolism, and toxicity,” Metal Ions in Life Sciences, vol. 7, pp. 231–265, 2010. View at Google Scholar

54. N. C. Papanikolaou, E. G. Hatzidaki, S. Belivanis, G. N. Tzanakakis, and A. M. Tsatsakis, “Lead toxicity update. A brief review,” Medical Science Monitor, vol. 11, no. 10, pp. RA329–RA336, 2005. View at Google Scholar

55. L. E. Wittmers Jr., A. C. Aufderheide, J. Wallgren, A. Alich, and G. Rapp, “Lead in bone. IV. Distribution of lead in the human skeleton,” Archives of Environmental Health, vol. 43, no. 6, pp. 381–391, 1988. View at Google Scholar

56. IPCS (International Programme on Chemical Safety), “Cadmium—Environmental Health Criteria 134,” World Health Organization, Geneva, Switzerland, 1992,

57. A. Menke, P. Muntner, E. K. Silbergeld, E. A. Platz, and E. Guallar, “Cadmium levels in urine and mortality among U.S. adults,” Environmental Health Perspectives, vol. 117, no. 2, pp. 190–196, 2009.View at Publisher ·View at Google Scholar · View at PubMed