From: imim@carson.u.washington.edu (Roger Lord)
Newsgroups: sci.med.aids
Subject: AIDS/HIV-mercury connection
Date: 20 Dec 92 06:11:09 GMT
Organization: University of Washington, Seattle
Note: Copyright 1992, Dan R. Greening. Non-commercial reproduction allowed.
Archive-Number: 6657


     Some months ago, I asked some questions regarding the possible 
AIDS-Mercury connection and was 'flamed' and lost interest in this 
newsgroup (and even how to logon).  But I have recovered and am presenting a
few of the journal article references that led to those questions.
They are:     

A.  Mercury amalgams have very much studied corrosion rates (1).  

B.  If the mother has amalgams, her unborn child will absorb mercury (2).  

C.  The body has many channels for the methylation of mercury (3).  

D.  Methylmercury suppresses the body's natural killer cells or T-cells (4).  

E.  Mercury stays in the body for a long time (5).

F.  AIDS patients have suppressed T-cells (6).  

     This also suggests that if the environment (or mouth) is immunosuppresent,
the incidence of AIDS/HIV may be high.  Africa is the biggest example with over
60% of the AIDS/HIV cases. 
     In conclusion, the above suggests that an HIV carrying person living in a
developed country may benefit from amalgam removal and chelation therapy.  
Amalgam removal will decrease the source of mercury.  Chelation therapy (if 
done correctly) will decrease the body burden of mercury.  If no amalgams 
(false teeth or too young), only chelation applies.  I would be very pleased 
if the above helps (cures?) people with the HIV virus and/or AIDS.  These 
arguments can be generalized to environmental pollutants that affect man.  

Notes:All of the notes are from the nationally available database "MEDLine" or
its sister database "MEdline BacK issues".

1)
AU   Brune-D.
TI   Metal release from dental biomaterials.
RF   REVIEW ARTICLE: 114 REFS.
SO   Biomaterials.  1986 May.  7(3).  P 163-75.
LG   Eng.
AB   Levels of corrosion products released from dental alloys in natural
     or synthetic saliva, i.e. from amalgams, cobalt, gold, nickel, iron,
     or titanium based alloys have been surveyed. The amounts of Ag, Au,
     Cd, Co, Cr, Cu, Hg, Mo, Ti or Ni released from such alloys, either in
     vitro or in vivo during animal tests or during clinical usage have
     been compiled. The quantities released have been adapted to a
     'standard restored man' with a specified number of restorations or a
     specified construction with a defined surface area, and compared to
     man's food and drink intake of similar elements. This was done as one
     approach to a security analysis of wearing dental alloys. In view of
     the assessment of extensive corrosion testing using electrochemical
     methods, rather scarce information seems presently available
     pertinent to release kinetics of specific elements in various
     biological environments like saliva or saliva substitutes. Several
     examinations indicate that mercury released from amalgams could be a
     substantial part of man's daily intake of this element, e.g. in the
     initial period following insertion, as well as on a long-term basis.
     From a copper amalgam cadmium could be released in vitro in amounts
     close to food and drink intake. The mercury release from the amalgam
     surface seems to be strongly influenced by the interaction of
     mechanical forces, e.g. chewing, and seems to be released according
     to a cyclic pattern. From a base metal alloy with high nickel content
     nickel could be released in vitro at the same level as from food and
     drink intake. However, from cobalt based alloys the nickel release
     seems insignificant in this context. The elemental release from the
     other alloys seemed to be far below the intake of similar elements
     from food and drink. Release under static and dynamic conditions has
     been discussed.
AA   Author
MJ   BIOCOMPATIBLE-MATERIALS: me.  DENTAL-MATERIALS: me.  METALS: me.
MN   ANIMAL.  BIOCOMPATIBLE-MATERIALS: to.  CORROSION.  DENTAL-ALLOYS: me.
     DENTAL-ALLOYS: to.  DENTAL-MATERIALS: to.  HUMAN.
     HYPERSENSITIVITY: et.  IN-VITRO.  METALS: to.  SALIVA: me.
SJ   METALS: me.
SN   ANIMAL.  CORROSION.  HUMAN.  HYPERSENSITIVITY: et.  METALS: to.
     SALIVA: me.
PT   JOURNAL-ARTICLE.  REVIEW.
RN   0 (Dental Materials).  0 (Metals).
JC   A4P.
SB   M.
IS   0142-9612
YR   86

2)
AU   Mottet-N-K.  Shaw-C-M.  Burbacher-T-M.
TI   Health risks from increases in methylmercury exposure.
RF   REVIEW ARTICLE: 55 REFS.
SO   Environ-Health-Perspect.  1985 Nov.  63.  P 133-40.
LG   Eng.
AB   Our present knowledge of the human health effects of methylmercury
     exposure is derived from study of major outbreaks of human poisonings
     in Japan and Iraq and experimental studies on primates. Methylmercury
     readily passes through such physiological barriers as the blood-brain
     barrier, blood-testes barrier, and the placenta. Its major
     pathological effects are on the nervous and reproductive systems and
     the developing embryo/fetus. The neurotoxicity of methylmercury is
     well established in both humans and non-human primates. Lesions in
     the cerebral and cerebellar gray matter consist of necrosis and lysis
     of neurons, phagocytosis and gliosis. The changes are most prominent
     in the deep sulci and may have a vascular component. A late effect is
     cerebral atrophy. At high dose levels the liver, kidneys, and other
     organs may also have degenerative changes. Although not yet described
     in humans, a major effect of exposure of female primates is an
     adverse effect on pregnancy. Maternal female M. fascicularis blood
     mercury levels above 1 ppm are associated with a decreased pregnancy
     rate and increased abortion rate. To date our experimental data lack
     sufficient numbers to detect infrequent pregnancy effects below 1
     ppm. Preliminary studies also reveal that methylmercury may also
     decrease the number and function (swim speed) of sperm. Both human
     and primate studies demonstrate deleterious effects of methylmercury
     on the developing embryo/fetus. Autopsies on human and primate
     infants reveal retarded brain development and the occurrence of a
     cerebral palsy-like behavior in the newborns, whereas the mother may
     be free of signs and symptoms of methylmercury toxicity. The fetal
     blood level of mercury is higher than the maternal level.(ABSTRACT
     TRUNCATED AT 250 WORDS)
AA   Author
MJ   METHYLMERCURY-COMPOUNDS: to.
MN   ANIMAL.  COGNITION: de.  DOSE-RESPONSE-RELATIONSHIP-DRUG.
     ENVIRONMENTAL-EXPOSURE.  FEMALE.  FETAL-DEATH: ci.  HUMAN.  MALE.
     MENTAL-RETARDATION: ci.  NERVOUS-SYSTEM-DISEASES: ci.  PREGNANCY: de.
     SPERM-MOTILITY: de.  SPERMATOGENESIS: de.  SUPPORT-US-GOV'T-PHS.
SN   ANIMAL.  COGNITION: de.  FEMALE.  HUMAN.  MALE.  PREGNANCY: de.
     SPERMATOGENESIS: de.
PT   JOURNAL-ARTICLE.  REVIEW.
NO   ES00677.  ES07032.
JC   EI0.
SB   M.
IS   0091-6765
YR   85

3) 
AU   Trevors-J-T.
TI   Mercury methylation by bacteria.
RF   REVIEW ARTICLE: 28 REFS.
SO   J-Basic-Microbiol.  1986.  26(8).  P 499-504.
LG   Eng.
AB   Bacteria capable of methylating Hg2+ have been isolated from
     sediment, water, soil and the gastrointestinal tract of humans.
     However, very little is known about the physiology and genetics of
     the mechanisms controlling Hg2+ methylation. Mercury methylation can
     be either chromosomal or plasmid-encoded in bacteria. In addition,
     the extent of nonbiological methylation is not well understood in
     environmental samples, where there are numerous physical, chemical
     and biological factors that control the methylation process. It is
     known that methylation of Hg2+ is mediated by a series of enzymatic
     reactions that are also responsible for the anaerobic evolution of
     methane. However, under highly reduced environments the reaction can
     also occur nonbiologically. It is possible that certain bacteria use
     methylation as a resistance/detoxification mechanism.
AA   Author
MJ   BACTERIA: me.  MERCURY: me.  METHYLMERCURY-COMPOUNDS: me.
MN   BACTERIA: ge.  CHROMOSOMES.  GENES-BACTERIAL.  HUMAN.  METHYLATION.
     PLASMIDS.  SUPPORT-NON-US-GOV'T.
SJ   BACTERIA: me.  MERCURY: me.
SN   BACTERIA: ge.  CHROMOSOMES.  HUMAN.  METHYLATION.  PLASMIDS.
PT   JOURNAL-ARTICLE.  REVIEW.
RN   7439-97-6 (Mercury).
JC   JOT.
SB   M.
IS   0233-111X
YR   86

4)
AU   Shenker-B-J.  Berthold-P.  Decker-S.  Mayro-J.  Rooney-C.  Vitale-L.
     Shapiro-I-M.
IN   Department of Pathology, University of Pennsylvania School of Dental
     Medicine, Philadelphia 19104-6002.
TI   Immunotoxic effects of mercuric compounds on human lymphocytes and
     monocytes. II. Alterations in cell viability.
SO   Immunopharmacol-Immunotoxicol.  1992.  14(3).  P 555-77.
LG   Eng.
AB   The major goal of this investigation was to examine the cytotoxic
     properties of both HgCl2 and MeHgCl, in terms of their ability to
     alter human T-cell and monocyte viability. Following treatment with
     HgCl2 (0-20 micrograms/ml) or MeHgCl (0-2 micrograms/ml), there was
     minimal reduction in lymphocyte viability at 1-4 hr. However, after
     exposure to mercury for 24 hr, cell death was apparent. In
     comparison, monocytes exhibited significant loss of viability during
     the early exposure periods. MeHgCl was approximately 5-10 times more
     potent than HgCl2. Other indicators of cell death were also
     determined. Measurement of the energy charge ratio indicated profound
     changes in cellular energy conservation. Electron microscopic
     analysis of cells treated with mercury revealed early nuclear
     alterations characterized by hyperchromaticity, nuclear fragmentation
     and condensation of nucleoplasm. In concert with these nuclear
     changes, there was destruction of cytoplasmic organelles with loss of
     membrane integrity. Studies of phospholipid synthesis by mercury
     treated cells confirmed that there were alterations in membrane
     structure. Thus, there was a decrease in total phosphatide synthesis
     by treated cells. Moreover, monocyte phospholipid synthesis appeared
     to be more sensitive to the presence of mercury then lymphocytes.
     Finally, both forms of mercury caused a rapid and sustained elevation
     in the intracellular levels of Ca++. These morphological and
     biochemical changes are consistent with the notion that mercury
     initiates cytotoxic changes associated with programmed cell death.
AA   Author
MJ   LYMPHOCYTES: de.  MERCURIC-CHLORIDE: to.
     METHYLMERCURY-COMPOUNDS: to.  MONOCYTES: de.
MN   ANIMAL.  CALCIUM: me.  CELL-DEATH: de.  ENERGY-METABOLISM: de.
     IN-VITRO.  LYMPHOCYTES: cy.  LYMPHOCYTES: me.  MERCURIC-CHLORIDE: ad.
     METHYLMERCURY-COMPOUNDS: ad.  MICROSCOPY-ELECTRON.  MONOCYTES: cy.
     MONOCYTES: me.  PHOSPHOLIPIDS: me.  RATS.  SUPPORT-US-GOV'T-PHS.
SJ   LYMPHOCYTES: de.  MONOCYTES: de.
SN   ANIMAL.  CALCIUM: me.  LYMPHOCYTES: cy.  LYMPHOCYTES: me.
     MONOCYTES: cy.  MONOCYTES: me.  PHOSPHOLIPIDS: me.  RATS.
PT   JOURNAL-ARTICLE.
RN   0 (Phospholipids).  115-09-3 (methylmercuric chloride).  7440-70-2
     (Calcium).  7487-94-7 (Mercuric Chloride).
NO   DE 08587.  DE06014.
JC   IAI.
SB   M.
IS   0892-3973
YR   92

5) 
        Author: Ingalls-T-H.

 Article Title: Epidemiology, etiology, and prevention of multiple sclerosis. 
                Hypothesis and fact.

        Source: Am-J-Forensic-Med-Pathol.  1983 Mar.  4(1).  P 55-61.

      Language: Eng.

      Abstract: Slow, retrograde seepage of ionic mercury from root canal or
                Class V amalgam fillings inserted many years previously,
                recurrent caries and corrosion around filling edges, and the
                oxidizing effect of the purulent response may lead to
                multiple sclerosis in middle age.  Epidemiologic studies of
                MS consistently reveal more neurological disease in the
                north, inferentially because there may be less caries and
                therefore fewer fillings done in the south.  Clinical and
                epidemiologic data also suggest that a second heavy metal,
                lead, may operate almost interchangeably with mercury. 
                Possibly, cases of unilateral MS derive from mercury-amalgam
                fillings in ipsolateral teeth, whereas the generalized
                disease may result from ingestion or inhalation of volatile
                mercury or exhaust fumes of lead additives to gasoline.  The
                forensic and preventive-medical challenge is to identify,
                monitor, and resolve questions of hidden heavy metal hazards
                in a high technology society, especially those of lead and
                mercury.  Further clinical-epidemiologic and basic science
                studies of heavy metal assays in whole blood, CNS tissues,
                packed cells, and serum are warranted.  Prevention awaits
                further testing of the hypothesis and experience with
                substitute filling materials.

  Author Abst.: Author

    MeSH Terms
         Major: DENTAL-AMALGAM: ae.  MULTIPLE-SCLEROSIS: ci.
         Minor: CLIMATE.  HUMAN.  LEAD-POISONING: et.  MERCURY-POISONING: et. 
                MULTIPLE-SCLEROSIS: ep.  MULTIPLE-SCLEROSIS: mo. 
                SUPPORT-NON-US-GOV'T.

Publication Tp: JOURNAL-ARTICLE.

 CAS Reg. Num.: 8049-85-2 (Dental Amalgam).

  Journal Code: 3HC.

Journal Subset: M.

Publication YR: 83

 Index Medicus: 8307

                         ----- End of Citation -----

6)
AU   Callahan-L-N.  Roderiquez-G.  Mallinson-M.  Norcross-M-A.
IN   Retrovirology Section, Food and Drug Administration, Bethesda, MD
     20892.
TI   Analysis of HIV-induced autoantibodies to cryptic epitopes on human
     CD4.
SO   J-Immunol.  1992 Sep 15.  149(6).  P 2194-202.
LG   Eng.
AB   Antilymphocyte antibodies, including autoantibodies to CD4, have been
     reported in AIDS patients and are postulated to contribute to T cell
     depletion and immunologic dysfunction. In this paper, we characterize
     and localize binding sites of human anti-CD4 autoantibodies from a
     number of HIV+ patients. Epitope mapping by ELISA and Western
     blotting, together with cross-competition experiments, showed that
     common autoepitopes were localized to at least two topographically
     separate sites on the fourth domain of sCD4. These sites were
     partially dependent on the carboxyl terminus of the soluble molecule
     and were not exposed on full length membrane CD4, even under
     denaturing Western blotting conditions. Peptide screening identified
     peptides from the fourth and third domains that were recognized by
     several, but not all, anti-CD4 serum samples. Soluble CD4
     affinity-purified antibodies were predominantly IgG1 and were not
     induced to bind mCD4 after gp120 binding to T cells. Analysis of HIV
     seroconversion panels showed that the appearance of anti-CD4
     antibodies followed HIV seroconversion by 6 to 12 months and
     paralleled anti-gp120 reactivity. This suggested a correlation
     between immune reactivity to envelope and anti-CD4 antibody
     production. Together, the data indicate that human anti-CD4
     antibodies recognize cryptic conformational and linear epitopes on a
     cleaved form of CD4. These findings suggest that HIV may induce
     abnormal cleavage of full length CD4, thereby exposing immunogenic
     self epitopes normally hidden from humoral and cellular immune
     interactions. This model of abnormal processing of self Ag has
     general implications for autoantigen exposure in other autoimmune
     disorders.
AA   Author
MJ   ANTIGENS-CD4: im.  AUTOANTIBODIES: im.  HIV-INFECTIONS: im.
MN   AMINO-ACID-SEQUENCE.  ANTIBODY-SPECIFICITY.  ANTIGENIC-DETERMINANTS.
     ANTIGENS-CD4: ch.  HUMAN.  IGG: im.  MOLECULAR-SEQUENCE-DATA.
     PEPTIDES: ch.  PEPTIDES: im.  PROTEIN-CONFORMATION.
SJ   AUTOANTIBODIES: im.
SN   HUMAN.  IGG: im.  PEPTIDES: ch.  PEPTIDES: im.
PT   JOURNAL-ARTICLE.
RN   0 (Antigenic Determinants).  0 (Antigens, CD4).  0 (Autoantibodies).
     0 (IgG).  0 (Peptides).
JC   IFB.
SB   A.  M.  X.
IS   0022-1767
YR   92
    
Roger Lord  rlord@phast.phys.washington.edu; U. of WA;  FM-15; Seattle,WA 98195
                                             206-685-4725