Mercury

“Renal inner medullary collecting duct cells (mIMCD3) and human embryonic kidney cells (HEK293) were used for cytoscreening of thimerosal and mercury chloride (HgCl2). Thimerosal and HgCl2 acted in a concentration-dependent manner. In mIMCD3 cells the 24-h LC50 values for thimerosal, thiosalicylic acid, 2,2-dithiosalicylic acid, and 2-sulfobenzoic acid were 2.9, 2200, >1000, and >10,000 microM, respectively. The 24-h LC50 value for HgCl2 in mIMCD3 cells was 40 microM. In HEK293 cells, the 24-h LC50 value for thimerosal was 9.5 microM. These data demonstrate that the higher cytotoxicity produced by thimerosal on renal cells with respect to similar compounds without Hg may be related to this metal content. The present study also establishes mIMCD3 cells as a valuable model for evaluation of cytotoxicity of nephrotoxic compounds.”

“PURPOSE:
To report a case of unilateral total limbal stem cell (LSC) failure and corneal opacification secondary to thimerosal- and contact lens-induced ocular surface toxicity.

METHODS:
Interventional case report and review of the literature on thimerosal-induced ocular surface changes.

RESULTS:
A 49-year-old woman with a 2-year history of long-term soft contact lens wear developed unilateral total LSC failure and corneal opacification secondary to presumed thimerosal-induced toxicity and contact lens wear. At presentation, best-corrected visual acuities were 20/120 in the right eye and 20/15 in the left eye. The patient underwent a keratolimbal allograft and amniotic membrane graft followed by a penetrating keratoplasty. At the last follow-up, the right eye showed a clear corneal graft with a best-corrected visual acuity of 20/30.

CONCLUSIONS:
Thimerosal toxicity can lead to total LSC failure with secondary corneal vascularization and opacification. Keratolimbal allograft followed by penetrating keratoplasty can be successful in reconstructing the ocular surface in such cases.”

“Clarkson and Magos (2006) provide their perspectives on the toxicology of mercury vapor and dental amalgam. As scientists who are involved in preparing a German federal guideline regarding dental amalgam, we welcome additional scientific data on this issue. However, Clarkson and Magos do not present all the relevant studies in their review. The additional data provided here show that: (a) Dental amalgam is the main source of human total mercury body burden, because individuals with amalgam have 2-12 times more mercury in their body tissues compared to individuals without amalgam; (b) there is not necessarily a correlation between mercury levels in blood, urine, or hair and in body tissues, and none of the parameters correlate with severity of symptoms; (c) the half-life of mercury deposits in brain and bone tissues could last from several years to decades, and thus mercury accumulates over time of exposure; (d) mercury, in particular mercury vapor, is known to be the most toxic nonradioactive element, and is toxic even in very low doses, and (e) some studies which conclude that amalgam fillings are safe for human beings have important methodogical flaws. Therefore, they have no value for assessing the safety of amalgam.”

“We describe the case of a 28-year-old woman, who had been suffering for more than 5 years from severe fatigue, myofascial pain, obstipation, obesity of trunk, abdominal striae, oedema, tinnitus, folliculitis, and facial swelling. The patient also showed a secondary adrenocortical insufficiency. From the anamnesis we assumed that environmental factors could account for the symptoms. The therapy consisted of dietary advise, chelating agents, supplements, and acupuncture. Under this therapy the patient became completely symptom-free. No such case has ever been reported before. We report mainly on the CAM diagnostic and therapeutic procedures, which are discussed together with the assumed pathogenetic factors.”

“Currently, mercury has been identified as a risk factor of cardiovascular diseases among humans. Here, the authors tested the hypothesis that mercury modulates the activity of the endothelial lipid signaling enzyme, phospholipase D (PLD), which is an important player in the endothelial cell (EC) barrier functions. Monolayers of bovine pulmonary artery ECs (BPAECs) in culture, following labeling of membrane phospholipids with [32P]orthophosphate, were exposed to mercuric chloride (inorganic form), methylmercury chloride (environmental form), and thimerosal (pharmaceutical form), and the formation of phosphatidylbutanol as an index of PLD activity was determined by thin-layer chromatography and liquid scintillation counting. All three forms of mercury significantly activated PLD in BPAECs in a dose-dependent (0 to 50 microM) and time-dependent (0 to 60 min) fashion. Metal chelators significantly attenuated mercury-induced PLD activation, suggesting that cellular mercury-ligand interaction(s) is required for the enzyme activation and that chelators are suitable blockers for mercury-induced PLD activation. Sulfhydryl (thiol-protective) agents and antioxidants also significantly attenuated the mercury-induced PLD activation in BPAECs. Enhanced reactive oxygen species generation, as an index of oxidative stress, was observed in BPAECs treated with methylmercury that was attenuated by antioxidants. All the three different forms of mercury significantly induced the decrease of levels of total cellular thiols. For the first time, this study revealed that mercury induced the activation of PLD in the vascular ECs wherein cellular thiols and oxidative stress acted as signal mediators for the enzyme activation. The results underscore the importance of PLD signaling in mercury-induced endothelial dysfunctions ultimately leading to cardiovascular diseases.”

“In their investigation of chemical exposure in dental personnel, Lindbohm et al conclude by saying that there is a weak association between exposure to chemical agents and an increased frequency of spontaneous abortion. Based on their data, the authors propose in the Policy implications section that ‘‘In general, there is no need to restrict work in dental clinics during pregnancy’’. We would like to express our concerns about their statement before these results reach public health policy.”

Amalgam restorative material generally contains 50% mercury (Hg) in a complex mixture of copper, tin, silver, and zinc. It has been well documented that this mixture continually emits mercury vapor, which is dramatically increased by chewing, eating, brushing, and drinking hot liquids. Mercury has been demonstrated to have damaging effects on the kidney, central nervous system, and cardiovascular system, and has been implicated in gingival tattoos. While mercury amalgams may result in detrimental exposure to the patient, they can also be a danger in dental practices. In Europe, the federal governments of Norway, Finland, Denmark, and Sweden have enacted legislation requiring that dental patients receive informed consent information about the dental restorative material that will be used. In the United States, a few state governments have enacted informed consent legislation for dental patients receiving dental restorations. These state legislations were enacted by Maine, California, Connecticut, and Vermont. It is a sad tragedy that mercury is causing such health damage to many people. The American Dental Association has said for the past 150 years that the mercury in amalgam is safe and does not leak; however, no clinical studies were ever done and the Food and Drug Administration approved amalgam under a grandfather clause. Subsequent studies have shown this claim of safety not to be true. Over ten years ago, the Federation of American Societies for Experimental Biology Journal published a comprehensive article calling mercury restorative material a major source of mercury exposure to the U.S. population. The authors of this paper recommend that federal and state legislation be passed throughout our country to ensure that consent forms are given to patients receiving silver-mercury amalgam restorative material.

“Thimerosal is a mercury-containing preservative in some vaccines. The effect of thimerosal on human gastric cancer cells is unknown. This study shows that in cultured human gastric cancer cells (SCM1), thimerosal reduced cell viability in a concentration- and time-dependent manner. Thimerosal caused apoptosis as assessed by propidium iodide-stained cells and caspase-3 activation. Although immunoblotting data revealed that thimerosal could activate the phosphorylation of extracellular signal-regulated kinase, c-Jun NH2-terminal protein kinase, and p38 mitogen-activated protein kinase (p38 MAPK), only SB203580 (a p38 MAPK inhibitor) partially prevented cells from apoptosis. Thimerosal also induced [Ca2+](i) increases via Ca2+ influx from the extracellular space. However, pretreatment with (bis(o-aminophenoxy)ethane-N,N,N’,N’-tetraacetate)/AM, a Ca2+ chelator, to prevent thimerosal-induced [Ca2+](i) increases did not protect cells from death. The results suggest that in SCM1 cells, thimerosal caused Ca2+-independent apoptosis via phosphorylating p38 MAPK resulting in caspase-3 activation.”

“The question of what is leading to the apparent increase in autism is of great importance. Like the link between aspirin and heart attack, even a small effect can have major health implications. If there is any link between autism and mercury, it is absolutely crucial that the first reports of the question are not falsely stating that no link occurs. We have reanalyzed the data set originally reported by Ip et al. in 2004 and have found that the original p value was in error and that a significant relation does exist between the blood levels of mercury and diagnosis of an autism spectrum disorder. Moreover, the hair sample analysis results offer some support for the idea that persons with autism may be less efficient and more variable at eliminating mercury from the blood.”

“The aims of this work were to compare the effects of methyl mercury chloride and thimerosal on neurite/process outgrowth and microtubule proteins in differentiating mouse N2a neuroblastoma and rat C6 glioma cells. Exposure for 4h to sublethal concentrations of both compounds inhibited neurite outgrowth to a similar extent in both cells lines compared to controls. In the case of N2a cells, this inhibitory effect by both compounds was associated with a fall in the reactivity of western blots of cell extracts with monoclonal antibody T1A2, which recognises C-terminally tyrosinated alpha-tubulin. By contrast, reactivity with monoclonal antibody B512 (which recognises total alpha-tubulin) was unaffected at the same time point. These findings suggest that decreased tubulin tyrosination represents a neuron-specific early marker of mercury toxicity associated with impaired neurite outgrowth.”