Brief review of eye problems related to mercury

Brief review of eye problems related to mercury. (B. Windham)

From my experience I know of 5 eye problems related to mercury. There are probably

more. One eye problem mercury causes is chronic iritis‑ I don't know much

about that but it’s documented in the medical literature and someone else I know had it. Another is color vision; that’s also documented in the medical literature and several I know have had color vision improve after amalgam removal, including me.

I have Fuch's disease(clouding of cornea caused by deterioration/glumping

of endothelial cells in the cornea. Animal studies and in vitro studies

have shown mercury causes similar damage to endothelial cells in various

parts of the body due to deterioration and free radical effects. Since having my amalgams removed over the last 2 years, my opthamologist says that the deterioration of the endothelial layer of my corneas has slowed considerably compared to 2 years ago. My vision has also improved so much that I cannot see at all through my glasses that I got 4 years ago. My optomitrist who did the glasses and reexamined me was really surprised, said my vision had improved almost 50%.

Another eye problem related to mercury is dry eyes. Several clinics have had success with improvements after amalgam relacement. The other eye problem known to sometimes be related to mercury is macula degeneration. The buildup of mercury in the eye is similar to in Fuch’s, etc. and causes clouding and degeneration. Someone I know says a relative got better after amalgam replacement. The following are a few abstracts or references I’m aware of.

Bernie

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macular degenerationDegeneration of the macula lutea of the eye. Often caused by free radical or oxidation damage.

www.nutritionfocus.com/nutrition_supplementation/glossary/GlossaryM.html

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SEAFOOD/CATARACTSMethylmercury in seafood may cause lens clouding, contributing to cataract development. Optometrist Ben Lane noted that his cataract patients liked seafood, while those who didn't like fish were clear-eyed. A study of 17 patients revealed that the cataract patients had eaten salt water fish or shellfish at least once a week on the average, but those cataract-free reported using these foods an average of once every five weeks. The cataract patients showed far higher concentrations of mercury in their hair. Dr. Lane's study showed that the presence of 2.3 ppm or more of mercury in hair samples was related to a 23-fold increase in the risk of cataracts. Dr. Lane encourages his patients to eat such foods as garlic and pectin-rich foods such as apples to help remove the mercury, and to receive adequate, while avoiding excessive, amounts of vitamins A, C, and E.

Dr, Ben Lane, O.D., Methylmercury in seafood contributes to cataract development, Medical World News, December 20, 1982

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I would look into the possibility of mercury poisoining which is capable of causing both cataracts and light sensitivity. (So are other things.) I have seen many babies born with mercury poisoning (further exacerbated by the mercury in vaccinations.) from their mother's dental amalgams. I would get a Hair Mineral Analysis right away. Good luck.Steve Rochlitzrochlitz@wellatlast.com ******************************************************

Cataract reversal through mercury detox www.digitalnaturopath.com/treat/T33633.html

Mobilization AND excretion are required for mercury detoxification. Consuming foods high in sulfur such as garlic, onions, beans, and eggs or supplemental sulfur in the form of MSM can help move mercury around but it is only bound loosely and caution is advised. There have been reported cases of reversible cataract development from individuals mobilizing mercury without excreting it. Consult a qualified doctor for a detoxification protocol appropriate for you. Alan Thal, MD

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Rudolph CJ, Samuels RT, McDanagh EW. Cheraskin E. Visual Field Evidence of Macular Degeneration Reversal Using a Combination of EDTA Chelation and Multiple Vitamin and Trace Mineral Therapy.In: Cranton EM, ed. A Textbook on EDTA Chelation Therapy, Second Edition. Charlottesville, Virginia: Hampton Roads Publishing Company; 2001

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Dr. G. E. Poesnecker, Its Only Natural, 2001, http://www.oneflesh.org/only‑22.html

Disorders that Chelation Can Help

Following is a list of conditions successfully treated by chelation that has been assembled by physicians who did much of the early research work. Many of these problems are common and are generally considered incurable: scleroderma; digitalis intoxication; heavy-metal poisoning (especially acute plumbism); calcinosis (pipestem calcinosis of the vessels, prostatic calcinosis); vascular atheromatous disorders including atherosclerosis, atheromatous deposits, arteriosclerosis obliterans, peripheral vascular insufficiency with intermittent claudication, and acute brain syndrome secondary to cerebral ischemia secondary to calcific atherosclerosis; myocardial or coronary insufficiency; collagenosis; arteriosclerosis including cerebrovascular arteriosclerosis; arthritis including hypertrophic and rheumatoid; calcific tendinosis; calculi; diabetic retinopathy; multiple sclerosis; macular degeneration of the retina; cataracts; Parkinsonism; emphysema; poisonous snake and insect bites; calcified necrotic ulcers; heart valve calcification; hemochromatosis; calcific bursitis; calcified granulomas; and hypertension.

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Mercury accumulates in the uvea and retina of the eye.

Khayat A, Dencker L. Whole body and liver distribution of inhaled mercury vapor in the mouse: influence of ethanol and aminotriazole pretreatment. J Appl Toxicol. 1983 Apr;3(2):66-74

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Inorganic mercury has been found to be associated with cataract formation.Hachet E. Cataracts, Bull Soc Ophtalmol Fr. 1985 Nov;Spec No:87-107. &&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&&Dr. Victoria Buntine, Mercury Effects, Healthinasia Incorporated, 2001www.healthinasia.com/mercury.html

The problem with mercury is that it affects our nervous system. Mercury accumulates in what we call end organs, like kidneys, brain, thyroid and eyes, and this is why it is detected on hair analysis It may contribute to cataracts, headaches, numbness and tingling, irritability, joint pain and autism in kids, as well as chronic fatigue syndrome and general allergies. *******************************************************

Dr. D.A. Carroll, O.D.& Dr. B.C. Lane, Preventing mercury related cataracts,

www.medicalvisioncenter.com/prevention.html

Vitamin C also helps to pull out the toxic mercury that results from the consumption of large fish, such as tuna, swordfish and shark. Dr. Lane said that his 1982 study found that mercury, which would accumulate in the crystalline lens, resulted in the depression of enzymes such as superoxide dismutase and glutathione peroxidase. The latter is the primary enzyme that helps prevent mercury cataracts from forming. 'Organic mercury is the worst offender because it's able to penetrate membranes and get into organic tissues,' he said.

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Cavalleri A, Belotti L, Gobba FM, Luzzana G, Rosa P & Seghizzi P. Colour vision loss in workers exposed to elemental mercury vapour. Toxicology Letters 77(1‑3):351‑356 (1995)

ABSTRACT: "We evaluated colour vision in 33 workers exposed to elemental mercury (Hg) vapour and in 33 referents matched for sex age, alcohol consumption and cigarette smoking. The results were expressed as colour confusion index (CCI). In the workers urinary excretion of Hg (HgU) ranged

from 28 to 287 ug/g creatinine. Subclinical colour vision loss, mainly in the blue‑yellow range, was observed in the workers. This effect was related to exposure, as indicated by the correlation between HgU and CCI (r=0.488, P<0.001).

& Urban P, Gobba F, Nerudova J, Lukas E, Cabelkova Z, Cikrt M,.Color Discrimination Impairment in Workers Exposed to Mercury Vapor. Neurotoxicology. 2003 Aug;24(4-5):711-716;

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If you want to know something about

retinitis pigmentosa (or retinopathia pigmentosa) and mercury poisoning,

you should read the following two articles:

1. Olynyk F, Sharpe DH: Mercury poisoning in paper pica. (retinitis pigmentosa)

N Engl J Med 1982 Apr 29;306(17):1056‑1057

2. Uchino M, Tanaka Y, Ando Y, Yonehara T, Hara A, Mishima I, Okajima T, Ando M: Neurologic features of chronic minamata disease (organic mercury poisoning) and incidence of complications with aging. J Environ Sci Health B 1995 Sep;30(5):699‑715

Also: Arch Ophthalmol 1990 Jan;108(1):113‑117

Distributions of elements in the human retinal pigment epithelium.

Ulshafer RJ, Allen CB, Rubin ML

Department of Ophthalmology, College of Medicine, Univ. of Florida, Gainesville 32610.

Distributions of elements above the atomic number of sodium were mapped in the retinal pigment epithelia of eight human eyes. X‑ray energy spectra and maps were collected from cryofixed, freeze‑dried, and epoxy‑embedded tissues using energy‑dispersive x‑ray microanalysis. All eyes had high concentrations of phosphorus in the nuclei of retinal pigment epithelial cells. Melanosomes were rich in sulfur, zinc, calcium, and iron. Lipofuscin and cytoplasm contained only phosphorus and sulfur in detectable amounts. Drusen, when present, contained phosphorus and calcium. Six eyes had a prominent aluminum peak recorded from melanosomes, nuclei, and Bruch's membrane. In one pair of 90‑year‑old eyes, small, electron‑dense deposits

surrounded many melanosomes and contained mercury and selenium. Retinal pigment epithelial melanosomes may bind and accumulate metals and

other potentially toxic ions over time, preventing them from reaching the neural retina.

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Journal of Environmental Science and Health Part B Pesticides Food Contaminants and Agricultural Wastes 30(5): 699-715. 1995

Abstract: Tessier‑Lavigne M, Mobbs P, Attwell D, Invest Ophthalmol Vis Sci 1985 Aug;26(8):1117‑1123 “Lead and mercury toxicity and the rod light response”.

Lead and mercury have been reported to alter selectively the rod component of the electroretinogram, and to inhibit the phosphodiesterase in rod outer segments which may be responsible for generating the rods' light response. The authors have investigated the effect of lead and mercury on the voltage response to light of rods, and compared these effects with those of the phosphodiesterase inhibitor papaverine. Lead and mercury, like papaverine, slow the light response. In addition, papaverine increases the light response amplitude while lead decreases it. Mercury initially increases and then decreases the amplitude. The late decrease in amplitude “produced by mercury is associated with rod degeneration”: an effect which may mimic degenerative diseases in which the rod phosphodiesterase is insufficiently active. These results demonstrate that the changes of electroretinogram induced by lead and mercury can be accounted for by the changes in receptor potential these heavy metals produce. The changes in receptor potential seen are consistent with mercury inhibiting the rod phosphodiesterase, and with lead having an action in addition to phosphodiesterase inhibition.

PMID: 2991162, UI: 85260515

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God Zb Med Fak Skopje 1978;24:289‑291

[Changes in the crystalline lens of the eye in workers occupationally exposed to mercury vapors]. [Article in Serbo‑Croatian (Cyrillic)]

Delivanova S, Popovski P, Orusev T PMID: 757176, UI: 80092857

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Abstract

“Effect of the ophthalmic preservative thimerosal on human and rabbit corneal endothelium”.

Van Horn DL, Edelhauser HF, Prodanovich G, Eiferman R, Pederson HF

Widespread use of the mercurial‑containing preservative thimerosal as an antibacterial agent in ophthalmic drugs and solutions warranted an investigation into its possible cytotoxic effects on the functional and ultrastructural integrity of the corneal endothelium. No changes in corneal thickness were observed during 5 hours' perfusion of the endothelium of rabbit and human corneas with 0.0001 and 0.0005 percent thimerosal in glutathione bicarbonate Ringer's solution (GBR). Scanning electron

microscopy (SEM) and transmission electron microscopy (TEM) of the endothelium of the 0.0001 percent group revealed normal ultrastructure. SEM and TEM of the endothelium of corneas perfused with 0.0005 percent thimerosal for 5 hours revealed condensed mitochondria, cytoplasmic vacuoles, and cytoplasmic flaps at the apical end of the cellular junctions. Perfusion of higher concentrations (0.001 and 0.005 perecnt) of thimerosal in GBR resulted in increases in corneal thickness after 2 hours

and irreversible ultrastructural damage to the endothelial cells by 5 hours. Corneas perfused with 0.01 and 0.1 percent thimerosal in GBR showed a rapid and immediate increase in corneal thickness and endothelial cell death and necrosis within 1 hour. It is postulated that the mercury in thimerosal

becomes bound to the cell membrane protein sulfhydryl groups, causing an

increase in cellular permeability; These results suggest that the prolonged exposure of the corneal endothelium to thimerosal in the accepted antimicrobial dosage of 0.005 to 0.001 percent may result in functional and “structural damage to the endothelium”. *

PMID: 844986, UI: 77140310

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Garron LK, Wood IS, Spencer WH, Hayes TL. A clinical pathologic study of mercurlalentis medicamentosus. Trans Am Ophthalmol Soc 1977;74:295‑320

Thirty‑one patients who used eye drops containing the preservative, phenylmercuric nitrate for from 3 to 15 years, developed a brownish pigmentation of the

anterior capsule of the pupillary area. Light and electron microscopic

studies on two lenses demonstrated deposits of dense particulate material

resembling melanin pigment on and in the anterior capsule of the lens in

the area of the pupil. Special studies, including electron microprobe

analysis and neutron activation analysis established the presence of mercury in a lens with mercurialentis. No mercury was found in two lenses used as controls.

PMID: 867632, UI: 77196922

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Klein, CL; Kohler, H; Kirkpatrick, CJ.

Increased Adhesion and Activation of Polymorphonuclear Neutrophil Granulocytes to Endothelial Cells under Heavy Metal Exposure in Vitro. Pathobiology. 62(2):90‑98, 1994.

ABSTRACT: Heavy metals have been implicated in the mechanisms of endothelial damage. Influences of heavy metal ions on diverse cell types have been studied using a variety of in vitro and in vivo methods. Polymorphonuclear neutrophil granulocytes (PMNs) have physiological and pathological functions, including the modulation of adhesion to and destruction of endothelial cells (ECs).

PMNs were studied during interaction with human umbilical vein ECs under exposure to zinc, nickel and cobalt using an in vitro model. We studied adhesion processes with the help of a computer‑controlled image‑analyzing system and examined the activation of PMNs by quantification of leukotriene

B4 (LTB4) release. The biphasic effects of the valuated heavy metals on PMN‑EC adhesion, with stimulation at very high and very low molar concentrations, were observed. The release of LTB4 by PMNs increased during exposure to very low metal concentrations. The initiation of these important pathogenetic mechanisms of inflammation at very low metal ion concentrations, which give no

morphologic changes, must be regarded as potentially significant with respect to the toxic effects of heavy metals. BIO‑PROBE COMMENT: Damage to the inner lining of blood vessels (endothelium)

is widely regarded to be the initial step in the disease process that leads to cardiovascular disease. Although mercury was not included in this study, it is a heavy metal that has previously been shown to cause endothelial damage. The three metals examined in this study nickel, cobalt and zinc)

are all used in dental restorative materials. Research, published in peer‑reviewed dental journals, has demonstrated the release and bioavailability of nickel (and mercury). Cardiovascular disease has become widespread only since the 1920's, about the time of increased use of heavy metals in dental

therapy and long after humans consumed eggs, meat, milk, butter and cheese.(other studies documenting mercury damage to is available on the web: use EXCITE search engine or MEDLINE http:///www.nlm.nih.gov/)

Abstract

Exp Eye Res 1993 Nov;57(5):549‑555

Low levels of inorganic mercury damage the corneal endothelium.

Sillman AJ, Weidner WJ

Section of Animal Physiology, University of California, Davis 95616.

The effect of inorganic mercury on the integrity of the endothelium of isolated bullfrog (Rana catesbeiana) corneas was examined by spectrophotometric analysis of corneal uptake of the vital stain Janus green, and by both transmission (TEM) and scanning (SEM) electron microscopy. The uptake of

Janus green by the endothelium is dose related between 1.0 and 30.0 microM HgCl2. The effect of mercury is not altered by changes in external calcium concentration, nor is it influenced by the calcium ionophore A23187, indicating that inorganic mercury damages the corneal endothelium through a mechanism which does not involve competition with external calcium or interaction with calcium channels. TEM and SEM demonstrate significant ultrastructural damage to the endothelium exposed to inorganic mercury, including cellular swelling, increased vacuolization, focal denuding of

Descemet's membrane, and diminished integrity at the intercellular junctions.

PMID: 8282041, UI: 94109509

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Toimela TA, Tahti H. Effects of mercuric chloride exposure on the glutamate uptake by cultured retinal pigment epithelial cells. Toxicol In Vitro 2001 Feb;15(1):7‑12

Tampere University Medical School, FIN‑33014 University of Tampere, Finland.

The cytotoxicity of mercuric chloride and the effects of mercuric chloride on glutamate and calcium uptake and the factors regulating glutamate uptake were studied in retinal pigment epithelium (RPE) cell cultures. RPE cells isolated from pig eyes and human RPE cell line (D407) cells were cultured to confluency and further subcultured according to the test protocol in question. The cytotoxicity caused by 15 min of exposure to mercuric chloride (0.01‑‑1000 microM) was evaluated by WST‑1 assay based on the activity of mitochondrial dehydrogenases. [(3)H]Glutamate uptake was measured after the cells were exposed to 0.1‑‑100 microM mercuric chloride and the selected regulators of protein kinase C (PKC) pathway: PKC activator SC10, PKC inhibitor chelerythrine chloride, phospholipase A(2)/C inhibitor manoalide, tyrosine kinase inhibitor lavendustin A, competitive NMDA receptor antagonist AP7 and IP(3) receptor antagonist heparin. Intracellular calcium was monitored with Fluo‑3 probe starting immediately after the exposure to 1‑‑1000 microM mercuric chloride. Mercuric chloride showed concentration‑dependent effects on cell viability, on glutamate uptake and on intracellular calcium concentration. The results give some support to the concept that glutamate uptake is affected by PKC. The PKC inhibitor chelerythrine chloride decreased glutamate uptake by 25%, but the PKC activator SC10 could partly prevent the inhibitory effect of mercuric chloride. Lavendustin A, manoalide and heparin had smaller, but statistically significant, effects. All these substances act on mediators which can regulate the activity of PKC. However, PKC is not likely to be the only regulator of glutamate uptake. The rise observed in [Ca(2+)](i) may initiate various cellular events during mercury intoxication.

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Hum Toxicol 1987 May;6(3):253‑256

Prenatal and early postnatal intoxication by inorganic mercury

resulting from the maternal use of mercury containing soap.

Lauwerys R, Bonnier C, Evrard P, Gennart JP, Bernard A.

A case of slight renal tubular dysfunction associated with cataract and anaemia was diagnosed in a 3‑month‑old black boy in whom high levels of mercury were found in blood and urine. Several arguments suggest that the renal, ocular and haematological defects may have resulted from exposure to mercury during foetal life and the 1‑month lactation period due to the extensive use of inorganic mercury containing cosmetics by the mother.

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1: Bull Soc Belge Ophtalmol 1978;181:21‑37

[Cataract of toxic origin(mercury)] [Article in French]

Michiels J.

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Bull Soc Ophtalmol Fr 1985 Nov;Cataracts:87‑107

[Cataracts(mercury)].

[Article in French]

Hachet E.

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Oftalmol Zh 1974;29(7):501‑503

[Eye manifestations of chronic mercury poisoning].

[Article in Russian]

Fomicheva IV.

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Bull Environ Contam Toxicol 1991 Feb;46(2):230‑236

Inhibition of corneal epithelial cell migration by cadmium and mercury.

Ubels JL, Osgood TB

Mount Desert Island Biological Laboratory, Salsbury Cove, Maine 04672.

PMID: 2018869, UI: 91208463

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Klein, CL; Kohler, H; Kirkpatrick, CJ.

Increased Adhesion and Activation of Polymorphonuclear Neutrophil Granulocytes to Endothelial Cells under Heavy Metal Exposure in Vitro.

Pathobiology. 62(2):90‑98, 1994.

morphologic changes, must be regarded as potentially significant with respect to the toxic effects of heavy metals.

BIO‑PROBE COMMENT: Damage to the inner lining of blood vessels (endothelium) is widely regarded to be the initial step in the disease process that leads to cardiovascular disease. Although mercury was not included in this study, it is a heavy metal that has previously been shown to cause endothelial

damage. The three metals examined in this study nickel, cobalt and zinc) are all used in dental restorative materials. Research, published in peer‑reviewed dental journals, has demonstrated the release and bioavailability of nickel (and mercury). Cardiovascular disease has become widespread only

since the 1920's, about the time of increased use of heavy metals in dental therapy and long after humans consumed eggs, meat, milk, butter and cheese.

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Toxicology 1996 Mar 18;107(3):189‑200

Mercury accumulation in the squirrel monkey eye after mercury vapour exposure.

Warfvinge K, Bruun A

Department of Ophthalmology, University Hospital of Lund, Sweden.

Squirrel monkeys were exposed to mercury vapour at different concentrations and for different numbers of days. The calculated total mercury absorption ranged between 1.4‑2.9 mg (range of daily absorption 0.02‑0.04 mg). The monkeys were killed at different intervals after the end of exposure (range 1 month ‑ 3 years) and the eyes were enucleated. Eyes from four un‑exposed monkeys were used as control material. Mapping of the mercury distribution in the eye revealed that the non‑myelin‑containing portion of the optic disc was densely loaded with mercury deposits, which are mostly confined to the capillary walls and the glial columns. The white matter of the brain does not accumulate mercury at these exposure levels, which might suggest that the myelinization process inhibits the accumulation of mercury. The pigmented epithelium of the pars plicata of the ciliary body and of the retina contained a considerable amount of mercury. This finding indicates that mercury is trapped within the melanocytes, which keeps potentially dangerous material from reaching the neural retina. In addition, the retinal capillary walls were densely loaded with mercury deposits, even 3 years after exposure. It was also found that the inner layers of the retina accumulated mercury during a 3‑year period. It is known that the biological half‑time of mercury in the brain may exceed years. This seems also to be the case for the ocular tissue.

PMID: 8604479, UI: 96180636

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Toxicology 1988 Sep;51(1):67‑76

Enhanced electroretinogram in cats induced by exposure to mercury acetate.

Gitter S, Pardo A, Kariv N, Yinon U

Institute for Occupational Health, Maurice and Gabriela Goldschleger Eye Research Institute, Chaim Sheba Medical Center, Tel‑Hashomer, Israel.

The present study was undertaken in order to verify whether, and how, retinal functions are affected by subacute poisoning with organic mercury. Mercury acetate in various concentrations (0.025‑0.25 mg/kg per day) was injected subcutaneously every second day to adult cats (N = 20) throughout a 2.5‑4.0‑week period. The electroretinogram (ERG) was recorded and the Hg2+ concentrations in the blood were determined. In nearly 90% of the intoxicated cats an enhanced electroretinogram (scotopic b‑wave amplitude) was found as compared to its level in the normal control cats (N = 10). The latency of the ERG was found to be appropriately shorter, up to a maximal difference of nearly 20% in comparison to the controls. Hg2+ was present in the blood of the exposed cats during a 2.5‑month period following the exposure. It is concluded that exposure to mercury acetate induces a permanent increase in the excitability level of the cat's retina.

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Toxicology 1983 Jan;26(1):1‑9

A cell aggregation model for the protective effect of selenium and vitamin E on

methylmercury toxicity.

Kleinschuster SJ, Yoneyama M, Sharma RP

Histotypic aggregation of embryonic neural retinal cells was chosen as a test model to evaluate mercury toxicity. After 24 h rotational culture with methylmercury (CH3HgCl) at 4 microM, aggregation was completely inhibited. A dose‑response relationship between concentrations of methylmercury and final sizes of aggregates was found. Selenium (Na2SeO3) at concentrations of 1, 3 and 5 microM provided a protective effect for methylmercury (1 microM) toxicity. Vitamin E (DL‑alpha‑Tocopherol acetate) at concentrations 5, 7 and 10 microM also provided protection against the same concentration of methylmercury; however, it was less effective than selenium. Histotypic embryonal retinal cell aggregation may be a useful assay system for in vitro neurotoxic studies in morphogenesis.

PMID: 6829026, UI: 83147085

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Science 1979 Oct 5;206(4414):78‑80

Heavy metals affect rod, but not cone, photoreceptors.

Fox DA, Sillman AJ

Low concentrations of lead, mercury, or cadmium depress the amplitude of the rod receptor potential in the perfused bullfrog retina. Responses from the cones were not affected. The data implicate the rods as a lesion site in animals exhibiting scotopic vision deficits as a result of heavy metal poisoning.

PMID: 314667, UI: 80014468

K.Warfvinge et al, "mercury accumulation in the monkey eye after mercury vapour exposure. Toxicology, 1996, 107: 189‑200.

mercury from vapor exposure accumulates over time in the various parts of the eye.

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Kishimoto T, Ohno M, Yamabe S, Tada M

Methylmercury Injury of Cultured Human Vascular Endothelial Cells

Journal of Trace Elements in Experimental Medicine. 6(4):155‑162, 1993

Abstract The effect of methylmercury chloride (MeHg) on cultured human vascular endothelial (HVE) cells was investigated. Umbilical vein‑derived HVE cells were collected by enzymatic digestion with collagenase. At concentrations of 0‑50 mu M, MeHg had only barely detectable effects on cell viability. However, the viability of HVE cells decreased dose‑dependently at concentrations >100 mu M.

Morphologic examination by phase‑contrast microscopy revealed a markedly damaging effect of MeHg at concentrations exceeding 500 mu M. The cytotoxic effect of MeHg on DNA synthesis was also concentration‑dependent. These results suggest that HVE cells are susceptible to concentration‑dependent MeHg cytotoxicity and that MeHg could induce vascular endothelial injury, which may be involved in the pathogenesis of arteriosclerosis. (C) 1993 Wiley‑Liss, Inc. [References: 34]

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I have seen several abstracts related to eye degeneration and mercury , due to my friends father's eye degeneration, I researched abstracts for my friend to give to his father. I do not have any of them handy yet anymore, but I found 1‑2 from Sam Queen's Chronic Mercury Toxicity book(see anotated bibliog.) , and I found quite a few more when I researched glutathione and lipoic acid, in addition to mercury, and it has been proven that mercury depletes glutathione and lipoate by binding to the thiols in these 2 as well as inhibiting various important glutathione system enzymes.

I found the abstracts from Medline, additionally, some where in the Life Extension Foundation Magazine abstract sections, and the same can be found also from Medline. I am sorry that these days I do not have enough time to go fetch the abstracts for you. But, what I found from tbe abstracts, lipoate, NAC, GSH, E‑vitamin and C‑vitamin have the greatest potential to be used as a protective treatment against mercury also in all eye disease that are due to oxidative damage and thiol‑binding by mercury.

Plaase go to Medline at www.medscape.com, join them free, and then seach with "mercury" and "macular" or "lipoate" and "macular" or "glutathione" and "macular" and cross all the years down to 1980 at least, and you will fork many abstracst to read.

Hope this helps,Ray

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From: "Amy L. Riskedahl, O.D." <ariskedahl@seanet.com>

Subject: Re: Vision

Cataracts and macular degeneration are the two eye diseases most often

attributed to oxidative damage. Cataracts can be taken out surgically but macular

degeneration often can't be helped. The progression can be slowed with

large amounts of certain anti‑oxidants such as lutein.

The macula is the part of the eye that has the highest number of cones and thus the sharpest vision and the best color vision. Mercury and other things that cause oxidative damage can damge the macula over time.

Generally what you do to heal the body, heals the eye. Get rid of the mercury. Vit. C,