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Neurotoxicity of Dental Amalgam is Mediated by Zinc

¹ Dept. of Biomedical Sciences and
² Dept. of Endodontics, Marquette University, 561 N. 15th Street, Rm. 426, Milwaukee, WI 53201;

View larger version (242K): [in a new window]   Figure 1. Cortical cell cultures with amalgam (dark shadow on left) placed on culture insert acutely (A) and after 24 hrs (B). Scale bar = 50 µm.

View larger version (25K): [in a new window]   Figure 2. Amalgam toxicity, but not mercury toxicity, was blocked by the metal chelator, CaEDTA, while the mercury chelator, DMPS, blocked mercury toxicity but not amalgam toxicity. (A) Amalgam, 0.010 + 0.002 mg; DMPS, 100 µM 2,3-dimercaptopropane-1-sulphonate; CaEDTA, 1 mM calcium disodium ethylenediaminetetraacetate. Amalgam was placed in tissue culture inserts so that it was exposed to the same media as the cells but was not in direct physical contact with the cells. Bars show % cell death (mean + SEM, n = 12). (B) Hg; 5 µM HgCl2. Bars show % cell death (mean + SEM, n = 8-16). Cell death was quantified by the measurement of release of LDH, 24 hrs after the beginning of the insult. Sham wash values were subtracted, and results were scaled to the level measured in sister cultures exposed to 10 µM A23187 for 24 hrs (n = 100; this exposure induced near-complete cell death). * indicates significant difference from control amalgam or mercury toxicity.

View larger version (20K): [in a new window]   Figure 3. CaEDTA attenuated zinc (Zn) toxicity, but not tin (Sn), copper (Cu), or silver (Ag) toxicity. Zn, ZnCl2; Sn, SnCl2; Cu, CuCl2; Ag, AgNO3; CaEDTA, 1 mM calcium disodium ethylenediaminetetraacetate. Bars show % cell death (mean + SEM, n = 6-16) quantified by the measurement of LDH release (A,B,C) or trypan blue staining (D), 24 hrs after the beginning of the insult. Sham wash values were subtracted, and results were scaled to the level measured in sister cultures exposed to 10 µM A23187 for 24 hrs. * indicates significant difference from the control metal toxicity.