Mercury causes the immune system to dysfunction.
Ability to secrete, move, and eat invaders goes first. Some people develop
autoimmunity due to mercury. Enough immune damage and you can have AIDS
without HIV.
The following reports make it abundantly clear that mercury should never
be used as a dental or medical treatment.
"Polymorphonuclear phagocytosis and killing in workers exposed to
inorganic mercury"; Int. J. Immunopharmacol; 12:16:1011-7; 1994;
Dec; Perlingeiro RC; Queroz ML.
"The ability of nuetrophils to phagocytose and kill Candida species
as well as the splenic phagocytic function were investigated in workers
from a mercury-producing plant. In the nuetrophil phagocytosis study, two
species of Candida were used since in individuals with myleperoxidase deficiency
nuetrophils are unable to kill Candida albicans, while Candida psuedotropicalis
can be effectively lysed. Phagocytosis of both antigens and splenic phagocytic
function were normal in all the workers studied. However, following ingestion
of the organisms there was considerable reduction in the ability of nuetrophils
from exposed workers to kill both species of Candida, and this was not explained
by a mild impairment of phagocytosis. After improvement in the hygiene conditions
in the factory, a new evaluation was performed, 6 months later, in the same
workers and urinary mercury concentrations were determined monthly in each
worker. Despite a significant reduction in urinary mercury concentrations,
a greater impairment in the ability of neutrophils to kill C. albicans was
observed. The killing of C. psuedotropicallis presented no further impairment
when compared to the previous evaluation. These results suggest that impairment
of the lytic activity of the nuetrophils from workers with urinary mercury
concentrations within the safe level for exposed population is due, at least
in part, to some interference with myeloperoxidase activity. In addition,
the mercury-NADPH complex, once formed, could limit the reduced pyridine
nucleotides by NADPH-dependent enzymes such as NADPH oxidase, thereby inhibiting
the PMN respiratory burst."
"Mercury: god of TH2 cells ?"; Mathieson PW; Clinical Exp
Immunol; 102:2:229-30; 1995; Nov;
Review of Literature and Editorial
1. In lower doses, HgCl2 has potent effects on the immune system of rodents..immune
stimulation or immunosuppression depending on the strain of animal involved.
2. In susceptible animals HgCl2 induces autoimmunity, with rats of the kidney.
3. Route of exposure unimportant, inhaled mercury vapor produces same autoimmunity
as injected HgCl2 in susceptible rats.
4. Preferential activation of Th2 subset of helper T cells.
5. HgCl2 can induce apoptosis in T cells in vitro.
6. HgCl2 induces aggregation of cell surface proteins such as CD4, CD3,
CD45 ad Thy-1 on T cells in vitro.
7. Dramatic tyrosine phosphorlation of several cellular proteins...
8. More, very technical effects on intercellular chemicals, compounds etc...
9. Preferential Th2 activation may underlie asthma, allergic disease, and
some forms of autoimmunity.
"Immunotoxic effects of mercuric compounds on human lymphocytes
and monocytes. Immune Suppression of T-cell activation."; Immunopharmacol
Immunotoxical; 14:3, 1992, 539-53; Shenker BJ; Rooney C; Vitale L; Shapiro
IM; Department of Pathology, University of Pennsylvania School of Dental
Medicine.
Experiment, Findings and Facts
1. T-Cells treated with 0-1000 ng HgCl2, and 0-100 ng CH3HgCl.
2. Both created dose dependent reduction in T-cell proliferation.
3. Presence of monocytes required for reduction. Without, HgCl2 enhanced
proliferation of T-cells.
4. CH3HgCl was approximately 5-10 times more potent than HgCl2.
5. Mercury inhibited the ability of these cells to synthesize and secrete
IL-1.
6. Decrease in T-cell function indicates mercury-containing compounds are
immunotoxic at very low exposure levels.
7. Mercuric compounds have adverse effects on both nuetrophil and macrophage
function.
8. Low doses of mercury have a profound inhibitory effect on human T-lymphocyte
activation.
9. A high concentration of mercuric ions would be expected to be retained
at the cell membrane where they would serve to inactivate enzyme systems,
especially those that exhibit free thiol (sulphydral) groups.
10. While immunologic dysfunction has not been considered to be an overt
effect of mercury toxicity, it nonetheless may be a critical event.
"Comparison of the interaction of methylmercury and mercuric chloride
with murine macrophages"; Arch. Toxicol; 1993; 3:67:205-11; Christensen
MM; Ellerman-Eriksen S; RungbyJ; Mogenson SC.
Findings and Facts
1. Macrophage cultures treated with methylmercury resulted in decreased
cell viability in a concentration-dependent fashion.
2. Cell viability showed no difference between equimolar concentrations
of methylmercury and mercuric chloride.
3. Interferon synthesis was reduced in a concentration dependent manner
with either methylmercury or mercuric chloride.
4. Impairment of random migration and phagocytosis appeared with lower concentrations
of methylmercury.
5. Electron microscope of methylmercury exposed cells showed mercury deposits
in lysosomes, cytoplasm and nuclei.
6. Methylmercury is 100 times more toxic to animals than inorganic mercury,
partly due to differences in absorption and solubility.
7. As a result of phagocytic activity, macrophages are often exposed to
higher concentrations of toxic metals than other cells.
8. Mercury and cadmium inhibit macrophage release of toxic oxygen species.
9. Mercuric chloride inhibited interferon production at much lower concentrations
than migration and phagocytosis.
10. Inorganic mercury appears to move into the cells after damage to the
membrane barrier, while methylmercury can penetrate cells without damage
to the cell membrane.
"New aspects of murine coxsackie B3 myocarditis--focus on heavy
metals"; European Heart Journal; 1995, Dec; Ilblack NG; Lindh U;
Fohlman J; Friman G; 16: suppl O; 20-4.
Findings
1. Magnitude of inflammatory lesions in the hearts of coxsackie B3 (CB3)-virus
infected mice can be affected by methylmercury.
2. CH3Hg appeared to have a direct effect on immune cells that resulted
in changed natural killer cell activity and decreased mobilization of macrophages,
CD4+ and CD8+ cells into the inflammatory lesions.
3. Another detrimental effect of CH3Hg treatment was evident by an increased
calcium and decreased zinc content in the inflamed heart.
4. CH3Hg increased T-cell activity in the spleen, but the NK-cell activity
decreased both in the blood and the spleen.
"In vitro reactions of macrophages to metal ions from dental biomaterials";
Dental Materials; 11:239-245, July 1995; JC Wataha; CT Hanks; Z Sun.
Findings
1. Macrophages react adversely to metal ions at similar concentrations as
other cell types found in the oral cavity.
2. Concentrations which affect cell metabolism and protein production are
generally lower than those which kill the cell.
3. Non-lethal concentrations of metal ions may alter the secretion of protein
inflammatory mediators such as cytokines.
"Murine systemic autoimmune disease induced by mercuric chloride:
T helper cells reacting to self proteins."; Int Arch Allergy Immunol;
109:1:11-20 ;1996 Jan; Kubicka-Muranyi M; Kremer J; Rottmann N; Luben B;
Albers R; Bloksma N; Luhrmann R; Gleichmann E.
Findings
1. HgCl2 induces a CD4+ T-cell dependent systemic autoimmune disease in
susceptible strains of rats and mice.
2. In rats, autoreactive T cells were shown to be involved.
3. In mice attention focused on "Hg-specific" T-cells.
4. T-cells from donors short term exposed to HgCl2 didn't self attack, but
mounted a significant reponse to HgCl2 and HgCl2 bearing cells.
5. T-cells from donors long term treated with HgCl2 hardly reacted to HgCl2
and Hg containing spleenic proteins, responding vigorously to nuclei and
fibrillarin irrespective of whether these self constituents had been treated
with HgCl2 or not.
"Autoreactive T cells in mercury-induced autoimmune disease: in
vitro demonstration"; J Immunol, 137:8; 1986 Oct 15, 2548-54; Pelletier
L; Pasquier R; Hirsch F; Sapin C; Druet P.
1. Mercuric chloride induces in Brown-Norway rats an autoimmune disease
due to a T dependent polyclonal activation of B cells.
2. HgCl2-pretreated cells were injected into the footpads of normal recipients
of the same genetic strain.
3. These experiments demonstrate that HgCl2 induces autoreactive T cells,
and suggests that these cells may be responsible for the autoimmune disease.
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