iaomtlibrary

“Thimerosal is a mercury derivative used as a preservative and bacteriostatic agent. We report an immediate hypersensitivity reaction after skin testing with an adult influenza vaccine that seems to be due to thimerosal. The patient is a 31-year-old woman with seasonal allergic rhinitis and irritable bowel syndrome. She developed conjunctival erythema and local pain after using a thimerosal-containing contact lens solution 15 years before the evaluation. She then switched to and tolerated the same brand of contact lens solution without thimerosal.”

“The effects of 1 min-4 h exposures to four Hg compounds (mercuric chloride [HgCl2], methyl mercuric chloride [CH3HgCl], p-chloromercuribenzoate [p-CMB] and thimerosal [TMS; ethylmercurithiosalicylate]) on cell death, microtubules, actin, CD3 receptor expression, protein tyrosine phosphorylation (PTyr-P) and intracellular calcium ([Ca2+]i) levels were investigated in YAC-1 lymphoma cells using flow cytometry. YOPRO-1 (YP) and propidium iodide (PI) dye uptake indicated all forms of Hg tested were toxic at concentrations ranging from 25.8-48.4 microM, with two distinct patterns of effects. Early apoptosis was prolonged for CH3HgCl- and TMS-treated cells, with more than 50% remaining YP+/PI- after 4h. Both CH3HgCl and TMS induced complete loss of beta-tubulin fluorescence, indicative of microtubule depolymerization and inhibition of tubulin synthesis and/or beta-tubulin degradation, while F-actin fluorescence diminished to a lesser degree and only after loss beta-tubulin. CH3HgCl and TMS induced an almost immediate two-fold increase in CD3 fluorescence, with levels returning to baseline within minutes. With continued exposure, CD3 fluorescence was reduced to approximately 50% of baseline values. Both compounds also increased PTyr-P two- to three-fold immediately, with levels returning to baseline at 4h. Similarly, two- to three-fold increases in [Ca2+]i were noted after 1 min exposure. [Ca2+]i increased progressively, reaching levels five- to eight-fold greater than control values. In contrast, dye uptake was delayed with HgCl2 and p-CMB, although cell death proceeded rapidly, with almost all non-viable cells being late apoptotic (YP+/PI+) by 4h. p-CMB produced early reductions in F-actin, and after 4h, complete loss of F-actin with only partial reduction of total beta-tubulin was seen with both p-CMB and HgCl2. HgCl2 reduced CD3 expression and PTyr-P slightly within minutes, while p-CMB produced similar effects on CD3 only at 4h, at which time PTyr-P was increased two- to three-fold. Both compounds increased [Ca2+]i within minutes, though levels remained under twice the baseline concentration after 15 min exposure. With continued exposure, [Ca2+]i increased to levels two- to five-fold greater than control values. These findings indicate the two groups of Hg compounds may induce cell death by distinct pathways, reflecting interactions with different cellular targets leading to cell death.”

“The primary purpose of this review is to bring together much of the available research and literature that focuses on health issues associated with mercury in dental fillings, some of the basic science information that is known about how the body processes mercury, and to offer some observations from the practices of dentists removing dental mercury from their patients. We also hope this review will draw attention to the potential connections between mercury released from dental fillings and autoimmune diseases. Many autoimmune diseases are classified as diseases of unknown etiology; yet, the well-documented toxic effects of mercury may explain some of the symptoms observed in autoimmune diseases.”

“Nitric oxide (NO) participates in the regulation of many cell functions in the CNS, including modulation of ion channel function by direct changes in the channel protein structure, modulating permeability or gating kinetics. The mechanisms by which NO donors modulate sodium currents are protein and tissue specific. The present paper concerns sodium currents in the neuroblastoma N1E-115 cell line, applying whole-cell voltage clamp methods. Sodium currents were characterized in terms of the sensitivity to NO donors and the hydrophilic thiol oxidizer thimerosal. Parameters defining steady-state inactivation and activation, removal of inactivation and the voltage dependence of inactivation, were determined before and after thimerosal application. The results concerning the application of thimerosal showed blockade of the resting state, hyperpolarizing shifts of m(infinity) and h(infinity) curves, change in the voltage sensitivity and slower inactivating kinetics, tau(hf) and tau(hs) being affected in the same manner. The present results provide clear evidence for redox modulation of the sodium channel population in N1E-115 cells. Our results showed that the membrane-permeable alkylating agent (NEM) does not inhibit current reduction determined by thimerosal. We have reasons to suspect that the sodium channel population in N1E-115 cells differs in the proposed consensus sequence for nitrosylation or thimerosal cysteine oxidation.”

“BACKGROUND:

Urinary mercury concentrations are widely used as a measure of mercury exposure from dental amalgam fillings. No studies have evaluated the relationship of these measures in a longitudinal context in children.

OBJECTIVE:

We evaluated urinary mercury in children 8-18 years of age in relation to number of amalgam surfaces and time since placement over a 7-year course of amalgam treatment.

METHODS:

Five hundred seven children, 8-10 years of age at baseline, participated in a clinical trial to evaluate the neurobehavioral effects of dental amalgam in children. Subjects were randomized to either dental amalgam or resin composite treatments. Urinary mercury and creatinine concentrations were measured at baseline and annually on all participants.

RESULTS:

Treatment groups were comparable in baseline urinary mercury concentration (approximately 1.5 microg/L). Mean urinary mercury concentrations in the amalgam group increased to a peak of approximately 3.2 microg/L at year 2 and then declined to baseline levels by year 7 of follow-up. There was a strong, positive association between urinary mercury and both number of amalgam surfaces and time since placement. Girls had significantly higher mean urinary mercury concentrations than boys throughout the course of amalgam treatment. There were no differences by race in urinary mercury concentration associated with amalgam exposure.

CONCLUSIONS:

Urinary mercury concentrations are highly correlated with both number of amalgam fillings and time since placement in children. Girls excrete significantly higher concentrations of mercury in the urine than boys with comparable treatment, suggesting possible sex-related differences in mercury handling and susceptibility to mercury toxicity.”

“This study determined the level of mercury, lead, and zinc in baby teeth of children with autism spectrum disorder (n = 15, age 6.1 +/- 2.2 yr) and typically developing children (n = 11, age = 7 +/- 1.7 yr). Children with autism had significantly (2.1-fold) higher levels of mercury but similar levels of lead and similar levels of zinc. Children with autism also had significantly higher usage of oral antibiotics during their first 12 mo of life, and possibly higher usage of oral antibiotics during their first 36 mo of life. Baby teeth are a good measure of cumulative exposure to toxic metals during fetal development and early infancy, so this study suggests that children with autism had a higher body burden of mercury during fetal/infant development. Antibiotic use is known to almost completely inhibit excretion of mercury in rats due to alteration of gut flora. Thus, higher use of oral antibiotics in the children with autism may have reduced their ability to excrete mercury, and hence may partially explain the higher level in baby teeth. Higher usage of oral antibiotics in infancy may also partially explain the high incidence of chronic gastrointestinal problems in individuals with autism.”

“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.”