Background: Ingested mercury produces symptoms clinically similar to those in MS; there is a direct correlation between dental caries incidence and its onset. These relationships have led to speculation that mercury from amalgam may be an aetiological factor in MS where the oligodendroglial cells that facilitate nerve conduction are destroyed. Objectives: to test the hypotheses that mercury can have direct toxic and apoptotic effects on the survival of oligodendroglial cells in vitro. Methods: MO3.13, a human-human hybrid oligodendroglial cell line was used. A range of concentrations of metal chlorides (Hg, Cd, Cu, Au, Co, Cr and Ni) and two dental monomers (HEMA, TEGDMA) were added to the culture medium. Mitochondrial dehydrogenase activity (MTT), an index of viable mitochondria and hence cell survival, was used to measure relative toxicity. To determine the mode of cell death cells were treated for 24hrs with HgCl₂ then subjected to morphological and biochemical analysis. Activity of caspase enzymes was measured by cleavage of fluorescent substrates and by immunoblotting. Results: HgCl₂ was found to have a very potent toxic effect on MO3.13 (10-50 µM), as did Cd. Caspase activation was observed and morphological analysis showed that cells exposed to low concentrations of HgCl ₂ exhibited features of apoptotic cell death including shrinkage and condensation of chromatin. High doses of HgCl₂ (250 µM) revealed necrotic characteristics (cell swelling and lysis). Conclusion: mercury is extremely toxic to differentiated oligodendrocytes at relatively low concentrations and thus is potentially damaging in vivo.

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