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“The influence of exposure to inorganic mercury on the immune system was examined in 36 workers occupationally exposed to mercury vapor, 14 individuals with skin hypersensitivity to mercury compounds, 21 subjects with health disturbances allegedly caused by dental amalgam fillings (“amalgam disease”), and 39 healthy referents. Concentrations of mercury in blood and urine and some parameters judged to mirror different effects on the immune system were determined. The latter included, white blood cell differential counts, serum immunoglobulins and autoantibodies, and in vitro production of the cytokines interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF alpha). Virtually all of the immunologic parameters were within normal ranges and did not differ significantly between the groups. In the group sensitized to mercury, there was a reduction of the in vitro production of both TNF alpha and IL-1 compared with the reference group’s values. No significant correlations were noted between different mercury exposure estimates and the immunologic parameters.”

“Photoaffinity labeling with [alpha-32P]8N3GTP and [gamma-32P]8N3GTP was used to identify the guanine binding domain of the GTP regulatory site within glutamate dehydrogenase (GDH). Without photolysis, 8N3GTP mimicked the regulatory properties of GTP on GDH activity with 8N3GTP exhibiting a Ki of 5 microM while the Ki for GTP was about 0.6 microM. Under optimal photolabeling conditions saturation of photoinsertion with 1 microgram of GDH revealed an apparent Kd of 9 +/- 4 microM for [gamma-32P]8N3GTP. Photolabeling with this analog could be competitively inhibited with GTP with an apparent Kd of 12 +/- 2 microM. Other nucleotides such as ATP and NAD(P)H could not reduce the amount of photoinsertion as effectively as GTP. ADP could decrease photoinsertion, but only at much higher concentrations. NAD(P)+, GDP, AMP, and GMP had little effect on photoinsertion. Divalent cations Mg2+ and Ca2+ also reduced photoinsertion significantly while the monovalent K+ and Na+ ions had no effect. Aluminum(III)-chelate or iron(III)-chelate affinity chromatography and reversed-phase HPLC were used to purify photolabel-containing peptides generated with either trypsin or chymotrypsin. This identified a portion of the guanine binding domain within the GTP regulatory site as the region containing the sequence Ile439 to Tyr454. Photolabeling of this peptide was prevented 91% by the presence of 300 microM GTP during photolysis. Lys445 was not identified in sequence analyses of the photolabeled peptides. Also, trypsin was unable to cleave the photolabeled peptide at this site. These results suggest that Lys445 may be the residue modified by [alpha-32P]8N3GTP.”

“Mercury and mercury compounds are widely used in modern society, but only sparse data are available on their carcinogenicity. Methylmercury chloride causes kidney tumors in male mice. Mercury chloride has shown some carcinogenic activity in male rats, but the evidence for female rats and male mice is equivocal. Other mercury compounds and metallic mercury have not been tested adequately in experimental animals. Epidemiologic data are available for chloralkali workers, dentists and dental nurses, and nuclear weapons workers, three groups occupationally exposed to low levels of mercury and its compounds, but those highly exposed in the past, such as miners, or populations which have suffered massive environmental exposure have not been adequately studied. However, the sparse epidemiologic data point toward the possibility of a risk of lung, kidney, and central nervous system tumors. Better data are needed on the carcinogenicity of mercury and mercury compounds in humans and experimental animals.”

“Dentistry has been portrayed as a high-risk profession in recent reports. A look at several areas of concern, however, shows that the field is no more hazardous than any other profession–and less than most.”

“Mercury levels (micrograms/mg dry weight) in dental plaque from amalgam and enamel surfaces in human subjects with amalgam restorations were (range, mean, SD) 0.5-1.31, 0.72, 0.34 and 0.01-0.54, 0.2, 0.19, respectively. The levels of mercury in plaque from amalgam surfaces were significantly higher than those from plaque on enamel (p < 0.001). No mercury was detected in plaque from subjects without amalgam restorations. The mean level of mercury in a 24-hour collection of plaque was 2 micrograms (median, 1.8 micrograms), an amount close to those calculated by other workers (1.2-1.7 micrograms) for the amount of mercury liberated in the mouth from amalgam restorations in 24 h. Freshly prepared amalgam liberated relatively large amounts of mercury into culture broth in the first 24 h of exposure; subsequently, the levels declined except in the presence of Streptococcus mutans. In vitro, biofilms of Streptococcus mutans facilitated the release of mercury from freshly prepared amalgam, in what appeared to be a cyclical fashion. Amalgam aged for two years did not release mercury, even when supporting the growth of an S. mutans biofilm. The resistance of aged amalgam was attributed to the presence of a passive tarnish layer. The mercury released by the biofilm had an effect on the composition of the biofilm. The biofilms on fresh amalgam had significantly lower levels of carbohydrate (p < 0.001-p < 0.01) and protein (p < 0.001-p < 0.02) than did biofilms on aged amalgam and on control stainless steel wires.”

“In vitro there was no indication that either inorganic mercury (vapor or metallic) or hydrogen peroxide catalyzed a rapid formation of peroxides in a polyunsaturated fatty acid as linoleic acid. When mercury and hydrogen peroxide were combined in a solution of linoleic acid, a notable amount of peroxide was registered by thin layer chromatography. As hydrogen peroxide is an inevitable intermediate product of oxygen metabolism and also a component of the immunologic defense system, the interaction between mercury and hydrogen peroxide must be considered an important fact in knowledge of the mechanisms of mercury toxicity. When natrium selenite was added to a linoleic acid containing mercury, an initial rise in peroxidation was observed. In a few days, however, the increase in peroxidation turned to a decrease. We consider dental amalgam as a source of mercury, and, therefore, toxicologically unsuitable as a tooth filling material.”

“The findings presented here suggest a correlation between many health complaints and mercury amalgam fillings. Removal of amalgam fillings results in significant improvement of these symptoms. These same symptoms which are improved or eliminated in amalgam-removal patients are present but undiagnosed in the general population.”

“The 1993 US Department of Health and Human Services Report on Dental Amalgam was to address the continuing concerns about amalgam safety.”