Guest guest Posted April 5, 2001 Report Share Posted April 5, 2001 http://www.mercola.com/article/mercury/mercury_elimination.htm Mercury Toxicity and Systemic Elimination Agents ph Mercola, DO. Abstract This paper reviews the published evidence supporting amalgam toxicity and describes practical and effective clinical techniques that facilitate mercury elimination. A literature review is provided which documents effective mercury elimination strategies to reduce mercury toxicity syndromes. Considering the weight of evidence supporting mercury toxicity, it would seem prudent to select alternate dental restoration materials and consider effective mercury elimination strategies if mercury toxicity is present. Key Words: amalgam and mercury toxicity; DMPS; DMSA; chlorella; cilantro Mercury Exposure And Toxicity Is A Prevalent And Significant Public Health Threat. Chronic mercury exposure from occupational, environmental, dental amalgam, and contaminated food exposure is a significant threat to public health. Those with amalgam fillings exceed all occupational exposure allowances of mercury exposure of all European and North American countries. Adults with four or more amalgams run a significant risk from the amalgam, while in children as few as two amalgams will contribute to health problems. In most children, the largest source of mercury is that received from immunizations or that transferred to them in utero from their mother. Dental Amalgams Are A Major Source Of Mercury Toxicity A single dental amalgam filling with a surface area of only 0.4 sq.cm is estimated to release as much as 15 micrograms of mercury per day primarily through mechanical wear and evaporation.1 The average individual has eight amalgam fillings and could absorb up to 120 micrograms of mercury per day from their amalgams. These levels are consistent with reports of 60 micrograms of mercury per day collected in human feces. By way of contrast, estimates of the daily absorption of all forms of mercury from fish and seafood is 2.3 micrograms and from all other foods, air and water is 0.3 micrograms per day. Currently, Germany, Sweden and Denmark severely restrict the use of amalgams.1 A " silver " filling, or dental amalgam, is not a true alloy. Amalgams are made up of 50% mercury. The amalgam also consists of 35% silver, 9% tin, 6% copper and a trace of zinc.6 More than 100 million mercury fillings are placed each year in the U.S. as over 90% of dentists use them for restoring posterior teeth. The mercury vapor from the amalgams is lipid soluble and passes readily through cell membranes and across the blood brain barrier. The vapor serves as the primary route of mercury from amalgams into the body. It is clear that amalgam mercury transfers to human tissues, accumulates with time, and presents a potential health threat. The mercury escapes continuously during the entire life of the filling primarily in the form of vapor, ions but also abraded particles. Chewing, brushing, and the intake of hot fluids stimulates this release. Statements made by dental authorities which claim that the amount of mercury exposure encountered by patients from dental amalgams is too small to be harmful, are contradicted by the literature. Animal studies show that radioactively labeled mercury released from ideally placed amalgam fillings appear quickly in the kidneys , brain and wall of the intestines. The fact that mercury amalgam fillings are banned in some European countries is strong evidence of the clinical toxicity of this material. Any metal tooth restoration placed in the mouth will also produce electrogalvanic effects. When dissimilar metals are placed in the oral cavity they exert a battery-like effect because of the electroconductivity of the saliva. The electrical current causes metal ions go into solution at a much higher rate, thereby increasing the exposure to mercury vapor and mercury ions manyfold. Gold placed in the vicinity of an amalgam restoration produces a 10-fold increase in the release of mercury. Mercury's Long Half-Life In The Central Nervous System Mercury in the central nervous system (CNS) causes psychological, neurological, and immunological problems in humans. Mercury bonds very firmly to structures in the CNS through its affinity for sulfhydryl groups on amino acids. Other studies have shown that mercury is taken up in the periphery by all nerve endings and rapidly transported inside the axon of the nerves (axonal transport) to the spinal cord and brainstem. Unless actively removed, mercury has an extremely long half--life of somewhere between 15 and 30 years in the CNS.1 Mercury Toxicity Symptoms The overt clinical effects resulting from toxic exposure to mercury have been clearly described. The scientific literature shows that amalgam fillings have been associated with a variety of problems such as Alzheimer's Disease, autoimmunity, kidney dysfunction, infertility, polycystic ovary syndrome, neurotransmitter imbalances, food allergies, multiple sclerosis, thyroid problems, and an impaired immune system. Patients with many amalgam fillings will also have an increase in the prevalence of antibiotic resistant bacteria. Subclinical neuropsychological and motor control effects were also observed in dentists who had documented high mercury exposure levels. Amalgam use may also be related to fatigue, poor memory and certain psychological disorders. There has been a recent epidemic of autism in the US and many investigators believe that this may be partially related to the increased exposure infants have had to mercury through the preservative thimerosal that was included in nearly all vaccines until recently. The nervous system is more sensitive to mercury toxicity than any other organ in the body. Mercury has recently been documented to be associated with arrhythmias and cardiomyopathies as hair analysis showed mercury levels to be 20,000 higher in those with these cardiac abnormalities. Mercury exposure has also been associated with other neurological problems such as tremors, insomnia, polyneuropathy, paresthesias, emotional lability, irritability, personality changes, headaches, weakness, blurred vision, dysarthria, slowed mental response and unsteady gait.1 Systemic Mercury Elimination There are a number of agents that have been demonstrated to have clinical utility in facilitating the removal of mercury with someone who has demonstrated clinical signs and symptoms of mercury toxicity. The urine and feces are the main excretory pathways of metallic and inorganic mercury in humans.1 The most important part of systemic elimination is to remove the source of mercury. For most this involves amalgam removal. Individuals should seek a dentist who is specially trained in this area as improperly removed amalgam may result in unnecessarily high exposure to mercury. The following is a summary of the most effective agents that have been documented in the peer-reviewed literature. DMPS DMPS (Sodium 2,3-dimercaptopropane-1-sulfonate) is an acid-molecule with two free sulfhydryl groups that forms complexes with heavy metals such as zinc, copper, arsenic, mercury, cadmium, lead, silver, and tin. DMPS was developed in the 1950s in the former Soviet Union and has been used to effectively treat metal intoxication since the 1960s there. It is a water-soluble complexing agent. Because it had potential use as an antidote for the chemical warfare agent, ite, it was not available outside of the Soviet Union until 1978, at which time Heyl, a small pharmaceutical company in Berlin, Germany started to produce it. It has an abundance of international research data and an excellent safety record in removing mercury from the body and has been used safely in Europe as Dimaval for many years. DMPS is registered in Germany with the BGA (their FDA) for the treatment of mercury poisoning but is still an investigational drug in the United States. DMPS Can Be Used To Eliminate Mercury Systemically The use of DMPS to treat mercury toxicity is well established and accepted. DMPS has clearly demonstrated elimination effects on the connective tissue. The DMPS dose is 3-5 mg /kg of body weight once a month which is injected slowly intravenously over five minutes. DMPS-stimulated excretion of all heavy metals reaches a maximum 2-3 hours after infusion and decreases thereafter to return to baseline levels after 8 hours. DMPS Safety DMPS is not mutagenic, teratogenic or carcinogenic. Ideally intravenous DMPS should never be used in patients that still have amalgam fillings in place, although investigators have done this as diagnostically, as a one-time dose, without complications. DMPS appears in the saliva and may mobilize significant amounts of mercury from the surface of the fillings and precipitate seizures, cardiac arrhythmias, or severe fatigue. Even though DMPS has a high affinity for mercury, the highest affinity appears to be for copper and zinc and supplementation needs to be used to not avoid depleting these beneficial minerals. Zinc is particularly important when undergoing mercury chelation. DMPS is administered over a five-minute period since hypotensive effects are possible when given intravenously as a bolus. Other possible side effects include allergic reactions and skin rashes. DMSA DMSA (meso-2, 3-dimercaptosucccinic acid) is another mercury chelating agent. It is the only chelating agent other than cilantro and d-penicillamine that penetrates brain cells. DMSA removes mercury both via the kidneys and via the bile. The sulfhydryl groups in both DMPS and DMSA bind very tightly to mercury. DMSA has three distinct disadvantages relative to DMPS. First, DMPS appears to remain in the body for a longer time than DMSA. Secondly, DMPS acts more quickly than DMSA, probably because its distribution is both intracellular and extracellular. Thirdly, preparations of DMPS are available for intravenous or intramuscular use, while DMSA is available only in oral form. Since succinic acid is used in the citric acid cycle inside the cell, DMSA has been suspected for displacing mercury towards the inside of the cell after binding mercury somewhere on its way from the intestine to the succinic acid deficient cell. We propose therefore that DMSA be used late in the mercury elimination process, after the connective tissue mercury load has been reduced with DMPS. The standard dose of DMSA is 5-10 mg/kg twice a day for two weeks. The DMSA is then stopped for two weeks and then the cycle is repeated. Chlorella Algae and other aquatic plants possess the capacity to take up toxic trace metals from their environment, resulting in an internal concentration greater than those of the surrounding waters. This property has been exploited as a means for treating industrial effluent containing metals before they are discharged, and to recover the bioavailable fraction of the metal. Chlorella has been shown to develop resistance to cadmium contaminated waters by synthesizing metal-binding proteins. A book written for the mining industry, Biosorption of Heavy Metals, details how miners use these organisms to increase the yield of precious metals in old mines. The mucopolysaccharides in chlorella's cell wall absorb rather large amounts of toxic metals similar to an ion exchange resin. Chlorella also enhances mobilization of mercury compartmentalized in non?neurologic structures such as the gut wall, muscles, ligaments, connective tissue, and bone. High doses of chlorella have been found to be very effective in Germany for mercury elimination. Chlorella is an important part of the systemic mercury elimination program, as approximately 90% of the mercury is eliminated through the stool. Using large doses of chlorella facilitates fecal mercury excretion. After the intestinal mercury burden is lowered, mercury will more readily migrate into the intestine from other body tissues from where chlorella will effectively remove it. Chlorella is not tolerated by about one-third of people due to gastrointestinal distress. Chitosan can be effectively used as an alternative in these individuals. Chitosan makes up most of the hull of insects shellfish and also bind metals like mercury from the lumen of the intestines. Cilantro Omura determined that cilantro could mobilize mercury and other toxic metals rapidly from the CNS. Cilantro mobilizes mercury, aluminum, lead and tin stored in the brain and in the spinal cord and moves it into the connective tissues. The mobilized mercury appears to be either excreted via the stool, the urine, or translocated into more peripheral tissues. The mechanism of action is unknown. Cilantro alone often does not remove mercury from the body; it often only displaces the metals form intracellularly or from deeper body stores to more superficial structures, from where it can be easier removed with the previously described agents. The use of cilantro with DMSA or DMPS has produced an increase in motor nerve function. Potentiating Agents Adequate sulfur stores are necessary to facilitate mercury's binding to sulfhydryl groups. Many individual's sulfur stores are greatly depleted which impairs sulfur containing chelating or complexing agents, such as DMPS or DMSA, effectiveness as they are metabolized and utilized as a source of sulfur. Sulfur containing natural substances, like garlic and MSM (methylsulfonylmethane) may also serve as an effective agent to supply organic sulfur for detoxification. Fresh garlic is preferred as it has many other recently documented benefits. The garlic is consumed just below the threshold of social unacceptability, which is typically 1-2 cloves per day. Antioxidants Vitamin E doses of 400 I.U per day have been shown to have a protective effect when the brain is exposed to methyl-mercury.68 Selenium, 200-400 mcg daily, is a particularly important trace mineral in mercury elimination and should be used for most patients. Selenium facilitates the function of glutathione, which is also important in mercury detoxification. Some clinicians find repetitive high dose intravenous glutathione useful, especially in neurologically compromised patients. There is a suggestion in a rat model that lipoic acid may also be useful, but some clinicians are concerned about the potential of lipoic acid to bring mercury into the brain early in the stages of chelation, similar to DMSA and N-acetylcysteine (NAC), which has also been used in mercury chelation. Vitamin C is also a helpful supplement for mercury elimination. Some clinicians will use it intravenously in doses of 25-100 grams IV in preference to DMPS and DMSA. Hyaluronic acid (HA) is a major carbohydrate component of the extracellular matrix and can be found in the skin, joints, eyes and most other organs and tissues. HA is utilized in many chemotherapy protocols as a potentiating agent. HA is also being utilized for many novel applications in medicine. Personal experience has shown that the addition of 2 ml with the DMPS tends to improve the excretion of mercury by two to four fold with virtually no toxicity. Conclusion We have described the significant toxicities associated with mercury amalgams and treatment agents that both authors have used successfully over the past two decades to eliminate mercury and resolve many chronic health complaints. Considering the weight of evidence supporting amalgam toxicity it would seem prudent to select alternative dental restoration materials. ph Mercola, DO. Medical Director Optimal Wellness Center 1443 W. Schaumburg Schaumburg, IL 60194 mercola@... Dietrich Klinghardt, M.D., Ph.D. Medical Director American Academy of Neural Therapy 2802 E.Madison #147 Seattle, WA 98112 neuralt@... Bibliography 1. Toxicological Profile For Mercury. U.S.Department Of Health & Human Services, Agency for Toxic Substances and Disease Registry, March 1999 Published by Division of Toxicology/Toxicology Information Branch, 1600 Clifton Road NE, E-29, Atlanta, Georgia 3033 2. GM. Assessment of mercury exposure and rsks from dental amalgam. Medical Devices Bureau, Environmental Health directorate, 1995 Health Canada. http://ww.hc-sc.gc/main/drugs/zmfiles/english/issues/mercury_exposure.html. 3. on IA; Some electromchemical features of the in vivo corrosion of dental amalgams. J Appl Electrochem 1989;19: 301-310 4. Skare I, Engqvist A., Human exposure to mercury and silver released from dental amalgam restorations. Arch Environ Hlth 1994;49:384-394 5. World Health Organization. Environmental Health Criteria. 118, Inorganic Mercury (Friber I, ed) WHO Geneva 1991. 6. Berry TC, Nicholson J, Torendle K.; Almost two centuries with amalgam. Where are we today? J Am Dent Assn 1994;120:394-395 7. Lorschider, F, Vimy MJ, Summers, AO: Mercury exposure from " silver " tooth fillings: Emerging evidence questions a traditional dental paradigm. FASEB J 1995; 9:504?508 8. Lorscheider F, Vimy MJ: Evaluation of the safety issue of mercury release from dental fillings. FASEB J 1993;7:1432-1433 9. Bjorkman L, Sandborgh-Englund G, Ekstrand J. Mercury in salvia and feces after removal of amalgam fillings. Toxicol Apply Pharmacol 1997;144:156-162. 10. Svare CW, LC, Reinhardt JW, Boyer DB, et.al; The effects of dental amalgams on mercury levels in expired air. J Dent Res 1981;60:1668-1671 11. Vimy MJ, Lorscheider F; Intra-oral air mercury released from dental amalgam. J Dent Res 1985;64:10069-1071 12. Aronsson AM; Lind B, Nylander M, Nordberg M; Dental amalgam and mercury. Biol Metals 1989; 2:25-30 13. Hanson M, Pleva J: The dental amalgam issue. A review. J Experentia. 1991;47:479-22 14. Hahn LJ, Kloiber R, Leininzer RW, Vimy MJ, Lorscheider FI; Whole-body imaging of the distribution of mercury released from dental fillings into monkey tissues. FASEB J 1990;4:3256-3260 15. Zahnaerztl, Knappwost et al. Abgabe von Quecksilberdampf aus Dentalamalgamen unter Mundbedingungen. Welt/Reform 1985;94, 131-138 16. Nierenberg DW, Nordgren RE, Chang MB, et al. Delayed cerebellar disease and death after accidental exposure to dimethylmercury. N Engl J Med. 1998;338(23): 1672?1676 17. son TW; Mercury - an element of mystery. N Engl J Med. 1990;323:1137-1139 18. The toxicological profile of mercury. 1994 publication by the US Department of Health and Human Services (Agency for Toxic Substances and Disease Registry, Division of Toxicology; 1600 Clifton Road NE E-29, Atlanta, GA 30333). 19. Eggleston DW, Nylander M.; Correlation of dental amalgam with mercury in the brain. J Prost Dent 1987;58:704-707 20. Retrograde Axonal Transport of Mercury; Bjoern Arvidson Experimental Neurology 1987;98, 198-203 21. Inorganic Mercury is Transported from Muscular Nerve Terminals to Spinal and Brainstem Motorneurons: Bjoern Arvidson Muscle and Nerve 1992;15:1089-1094 22. Handbuch der Amalgamvergifung, Max Daunderer, Ecomed Verlag, Muenchen(1996) 23. son TW, Hursh IB, Sager PR, Sverson TLM: Mercury. In Biological Monitoring of Toxic Metals (son TW, Friberg L, Nordberg CF,, and Sager PR, eds) pp 199-246. Plenum, New York 1988. 24. Klassen CD. Heavy metals and heavy-metal antagonists. In: The Pharmacological Basis of Theraputics, 8th edition(Gilman AC, Rall TW, Niew AS, P, eds) pp. 1598-1602. Pergamon Press, New York 1990. 25. Hirsch F, Kuhn J, Ventura M, Vial MC, Fournie G, Druet P; Production of monoclonal antibodies. J Immunol 1986;136:3272-3276 26. Hultman P, Johansson U, Turley Sj, Lindh U, Enestrom S, Pollard KM; Adverse immunological effects and autoimmunity induced by dental amalgam and alloy in mice. FASEB J 1994;8:1183-1190 27. Biagazzi M, Pierlguigi E; Autoimmunity and heavy metals. Lupus 1994;3:449-453. 28. Nylander M, Frierg I, Lind B; Mercury concentrations in the human brain and kidneys in relation to exposure from dental amalgam fillings. Swed Dent J 1987;11:179-187 29. Dondero F, Lenzi A, Lombardo F, Gandini L; Therapy of immunologic infertiilty. Acta Eur Fertil 1991;22:139-145 30. Rowlands AS, Baird DD, Weinberg CP, Shore DL, Shy CM, Wilcos AJ. The effect of occupational exposure to mercury vapor on the fertility of female dental assistants. Occup Environ Med 1994;51:28-34. 31. Gerhard I, Monga B, Waldbrenner A, Runnebaum B Heavy metals and fertility. J Toxicol Environ Health 1998;21;54(8):593-611 32. Gerhard I, Frick A, Monga B: Diagnosis of mercury body burden. Clin Lab 1997;43:637-647 33. Duhr E, Pendergrasss C, Kasarskis E, Slevin J Haley B; Mercury induces GTP-tubulin interactions in rat brain similar to those observed in Alzheimer's disease. FASEB J 1991; 5:456. 34. Hultman P, Johansson U, Turle S,J, et al: Adverse immunological effects and autoimmunity induced by dental amalgam and alloy in mice. FASEB J 1994;8:1183-1190 35. Siblered TL, Kienholz E. Evidence that mercury from silver dental fillings may be an etiological factor in reduced nerve conduction velocity in multiple sclerosis patients. Journal of Orthomolecular Medicine 1997;12(3):169-172. 36. Pelletier L, Pasquier R, Rossert J, et al: Autoreactive T cells in mercury-induced autoimmunity. Ability to induce the autoimmune disease. J Immunol 1988;140:750-754 37. Summers AO, Wireman J, Vimy MI, Lorscheider FI, Marshall B, Levy SB, et al; Mercury released from dental Asilver@ fillings provokes an increase in mercury and antibiotic-resistant bacteria in oral and intestinal floras of primates. Antimicrob Agents and Chemother 1993;37:825-834 38. Escheverria D, Hever N, MD, Naleway CA, Woods JS Bittner AC; Behavioral effects of low level exposure to mercury among dentists. Neurotxicol Teratol 1995;17:161-168 39. Ngim CH: Chronic neurobiological effects of elemental mercury in dentists. Br J Indust Med 1992;49:782-790 40. Siblerud RL; The relationship between mercury from dental amalgam and mental health. Am J Psychotherapy 1989;18:575-587 41. Frustaci A, Magnavita N, Chimenti C, et. al; Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy. J Am Coll Cardiology 1999;33:1578-83 42. Chang YC, Yeh C, Wang JD. Subclinical neurotoxicity of merucyr vapor revcelaed by a multimodality evoked potential study of chloralkali workers. Amer J Ind Med 1995;27(2):271-279. 43. Yang Y-J, Huang C-C, Shih T-S, et al . Chronic elemental mercury intoxication:clinical and field studies in lampsocked manufacturers. 1994;Occup Environ Med 57(1):245-247. 44. son TW. Mercury. 1989; J Am Coll Toxicol 8(7):1291-1296. 45. Eley BM The future of dental amalgam: A review of the literature. Part 2: Mercury exposure in dental practice. Br Dent J 1997;182(8):293-7. 46. Petrunkin VE: Synthesis and properties of demercapto derivatives of alkylsulfonic acids. Toksikol mosc 1958;21: 53-59 47. -Alanis O, Garza-Ocanas L, Pineyro- A. Evaluation of urinary mercury excretion after administration of 2,3-dimercapto-1-propane sulfonic acid to occupationally exposed men. J Toxicol Clin Toxicol 1995;33(6):717-720 48. Aaseth J, sen D, Andersen O, Wickstrom E. Treatment of mercury and lead poisonings with dimercaptosuccinic acid and sodium dimercaptopropanesulfonate. 1995;120(3):853-854 49. Aposhian HV, Maiorino RM, M, et al Human studies with the chelating agents, DMPS and DMSA. J Toxicol Clin Toxicol 1992;30(4):505?528 50. Aposhian HV, Aposhia MM. Meso?2,3 dimercaptosuccinic acid: chemical, pharmacological and toxicological properties of an orally effective metal chelating agent. Annu Rev Toxicol 1990;30:279?306 51. Lorscheider FL, Vimy MJ. Evaluation of the saftey issue of mercury release from dental fillings. FASEB J 1993;7:432?1433 52. Aposhian VK: Mobilization of Mercury and Arsenic in Humans by Sodium 2,3 Dimercapto-1-propane Sulfonate (DMPS). Environ Health Perspect 1998;106(Suppl 4):1017-1025 53. Schiele R, Schaller KH, Welte D: Mobilization of mercury reserves in the organism by means of DMPS. Occup Med Soc Med Prevent Med 1989;24: 249-251 54. Belles M, DJ, Gomez M, Domingo JL, MM, Singh PK Assessment of the protective activity of monisoamyl meso-2,3-dimercaptosuccinate against methylmercury-induced maternal and embryo/fetal toxicity in mice. Toxicology 1996;106(1-3):93-97 55. Kostial K, Restek-Samarzija N, Blanusa M, Piasek M, Prester L, MM, Singh PK Racemic-2,3-dimercaptosuccinic acid for inorganic mercury mobilization in rats. J Appl Toxicol 1997;17(1):71-74 56. Gerhard I; Runnebaum B: Schadstoffe und Fertiliatatsstorungen Schwermetalle und Mineralstoffe. Geburtshilfe Frauenheillkd 1992;52:383-396, 509-515 57. Handbuch der Amalgamvergifung, Max Daunderer, Ecomed Verlag, Muenchen 1996 58. Sallsten G, Barregard L, Schutz A Clearance half life of mercury in urine after the cessation of long term occupational exposure: influence of a chelating agent (DMPS) on excretion of mercury in urine. Occup Environ Med 1994;51(5):337-342 59. Aposhian HV, Maiorino RM, - D, et al. Mobilization of heavy metals by newer, therapeutically useful chelating agents. Toxicology 1995;31;97(1-3):23-38 60. - D, Maiorino RM, Zuniga- M, et al Sodium 2,3-dimercaptopropane-1-sulfonate challenge test for mercury in humans: II. Urinary mercury, porphyrins and neurobehavioral changes of dental workers in Monterrey, Mexico. J Pharmacol Exp Ther 1995;272(1):264-274 61. Kostial K, Restek?Samarzija N, Blanusa M, Piasek M, MM, Singh PK Combined oral treatment with racemic and meso?2,3?dimercaptosuccinic acid for removal of mercury in rats. Pharmacol Toxicol 1997;81(5):242?244 62. AL. Dimercaptosuccinic acid (DMSA), a non?toxic, water?soluble treatment for heavy metal toxicity. Altern Med Rev. 1998;3(3): 199?207 63. Handbuch der Amalgamvergifung, Max Daunderer, Ecomed Verlag, Muenchen(1996) 64. Hurlbut KM, Maiorino RM, Mayersohn M, Dart RC, Bruce DC, Aposhian HV Determination and metabolism of dithiol chelating agents. XVI: Pharmacokinetics of 2,3-dimercapto-1-propanesulfonate after intravenous administration to human volunteers. J Pharmacol Exp Ther 1994;268(2):662-668 65. Zheng W, Maiorino RM, Brendel K, Aposhia HV. Determination and metabolism of dithiol chelating agents. Fundam Appl Toxicol 1990;14:598-607 66. Aposhian HV. Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate. Environ Health Perspect 1998;106 Suppl 4:1017-1025 67. Research data presented at the annual meeting of the Australasian Society of Oral medicine and Toxicology in Sydney, Australia, Sept.1998 68. H.B.Xue, W.Stumm, L.Sigg: The binding of Heavy Metals to Algal Surfaces, Water Res 1988;22, 917 69. Ahner, AB, Kong KS, Morell MM, Phytochelatin production in marine algea: An interspecies comparison. Limnol Oceanograph 1995;40: 649-657 70. Carr HP, et al. Characterization of the cadmium?binding capacity of Chlorella vulgaris. Bull Environ Contam Toxicol. 1998;60(3): 433?440 71. M. Tsezos: Biosorption of Radioactive Species, in: Biosorption of Heavy Metals, pp 45-50 editied by B.Volesky, CRC Press(1990) 72. M.Kraft: Bindungsverhalten von Arsen, Cadmium, Chrom, Quecksilber, Nickel und Blei an schwerverdauliche Lebensmittel und Lebensmittelkomponenten in kuenstlichem Magen-Darm-Saft. PhD Thesis. Institut fuer Hygiene, Sozial-und umweltmedizin der Ruhr-Universitaet Bochum, Germany, (1998) 73. Klinghardt, D: Amalgam/Mercury Detox as a Treatment for Chronic Viral, Bacterial, and Fungal Illnesses Explore! Volume 1997;8, No 3 74. M.Kraft: Bindungsverhalten von Arsen, Cadmium, Chrom, Quecksilber, Nickel und Blei an schwerverdauliche Lebensmittel und Lebensmittelkomponenten in kuenstlichem Magen-Darm-Saft. PhD Thesis. Institut fuer Hygiene, Sozial-und umweltmedizin der Ruhr-Universitaet Bochum, Germany, 1998 75. R.Muzzarelli, O.Tubertini: Chitin and chitosan on chromatographic supports and adsorbents for collection of metal ions from organic and aqueous solutions and sea water, Talanta, 1969;16, 1571 ff 76. Y.Subramanian, T.Yoshinar: Studies on the formation of chitin-metal complexes, Rep.No 27, Marine Sciences Center, Mc Gill Univ, Montreal (1974) 77. J.W.Park, M.O. Park: Mechanism of metal ion binding to chitosan in solution, cooperative inter- and intramolecular chelations. Bull.Korean Chem.Soc. 1984;5(3), 108 78. Omura Y, Beckman SL Role of mercury (Hg) in resistant infections & effective treatment of Chlamydia trachomatis and Herpes family viral infections (and potential treatment for cancer) by removing localized Hg deposits with Chinese parsley and delivering effective antibiotics using various drug uptake enhancement methods. Acupunct Electrother Res. 1995;20(3?4): 195?229 79. Omura Y, Shimotsuura Y, Fukuoka A, Fukuoka H, Nomoto T. Significant mercury deposits in internal organs following the removal of dental amalgam, & development of pre?cancer on the gingiva and the sides of the tongue and their represented organs as a result of inadvertent exposure to strong curing light (used to solidify synthetic dental filling material) & effective treatment: a clinical case report, along with organ representation areas for each tooth. Acupunct Electrother Res. 1996 ;21(2): 133?160. 80. Ewan KB, Pamphlett R Increased inorganic mercury in spinal motor neurons following chelating agents. Neurotoxicology 1996;17(2):343-349 81. Cha CW A study on the effect of garlic to the heavy metal poisoning of rat. J Korean Med Sci 1987;2(4):213-224 82. H.Wagner, A.Sendl: Baerlauch und Knoblauch - vergleichende chemische und pharmakologische Untersuchungen, Deutsche Apotheker Zeitung 130 Jahrg., Nr.33, 16.8.1990 83. The Miracle of MSM The Natural Solution for Pain. , S., Lawrence, RM, Zucker, M. Penguin Putnam, New York, NY 1999. 84. Chang, L.W , Gilbert,M and Sprecher,J: Modification of methylmercury neurotoxicity by vitamin E, Environ.Res. 1978;17:356-366 85. Yoneda S, Suzuki KT Toxicol Appl Pharmacol Detoxification of mercury by selenium by binding of equimolar Hg-Se complex to a specific plasma protein. 1997;143(2):274-280 86. Akesson I, Ingrid B; Status of mercury and selenium in dental personnel: Impact of amalgam work and own fillings. Arch Environ Health 1991;46(2):103-109 87. Johansson E: Selenium and its protection against the effects of mercury and silver. J Trace Elements 1991;5:273-274 88. Dirks M, Marvin J; Mercury excretion and intravenous ascorbic acid. Arch Environ Health 1994;49(1):49-52 89. Hill, CH. Interactions of vitamin C with lead and mercury. Ann N Y Acad Sci 1980;355:262-6 90. Yamini B, Sleight SD. Effects of ascorbic acid deficiency on methyl mercury dicyandiamide toxicosis in guinea pigs J Environ Pathol Toxicol Oncol 1984 Jul;5(4-5):139-50 91. Zorn NE, JT A relationship between vitamin B12, folic acid, ascorbic acid, and mercury uptake and methylation.Life Sci 1990;47(2):167-73 92. Sorg O, Schilter B, Honegger P, et. al. Increased vulnerability of neurones and glial cells to low concentrations of methylmercury in a prooxidant situation. Acta Neuropathol (Berl) 1998 Dec;96(6):621-7 93. Hultberg B, Andersson A, Isaksson A Thiol and redox reactive agents exert different effects on glutathione metabolism in HeLa cell cultures.Clin Chim Acta 1999 May;283(1-2):21-32 94. Crinnion WJ. Environmental medicine, part three: long-term effects of chronic low-dose mercury exposure Altern Med Rev 2000 Jun;5(3):209-23 95. Chen WY, Abatangelo G.Functions of hyaluronan in wound repair. Wound Repair Regen 1999;7(2):79-89 96. Delpech B, Girard N, Bertrand P, Courel MN, Chauzy C, Delpech Hyaluronan: fundamental principles and applications in cancer. J Intern Med 1997;242(1):41-8 97. Sutherland IW. Novel and established applications of microbial polysaccharides. Trends Biotechnol 1998;16(1):41-6 98. Knudson CB, Nofal GA, Pamintuan L, Aguiar DJ: The chondrocyte pericellular matrix: a model for hyaluronan-mediated cell-matrix interactions. Biochem Soc Trans 1999;27(2):142-7 Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.