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Influence of dental amalgam and heavy metal cations on in vitro interleukin-1β production by human peripheral blood mononuclear cells
The influence of dental amalgam and heavy metal cations on interleukin‐1β (IL‐1β) expression by peripheral blood mononuclear cells from healthy donors was studied. A marked decrease in the production of IL‐1β was caused by freshly prepared amalgam or amalgam‐conditioned culture medium, but not by am...
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Published in: | Journal of biomedical materials research 2000-07, Vol.51 (1), p.88-95 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | The influence of dental amalgam and heavy metal cations on interleukin‐1β (IL‐1β) expression by peripheral blood mononuclear cells from healthy donors was studied. A marked decrease in the production of IL‐1β was caused by freshly prepared amalgam or amalgam‐conditioned culture medium, but not by amalgam aged for 6 weeks. When metal cations were added as salts, Cu2+, Hg2+, and Ag+ at high concentrations (33.3 and 333.3 μM) were highly inhibitory. Among other heavy metal cations, Au3+, Pt4+, Ni2+, Pd2+, but not Ga3+ or Sn2+, inhibited IL‐1β production in a concentration‐dependent manner. Flow cytometry studies indicated that Hg2+ and Ag+ strongly reduced the percentage of CD14+ cells containing IL‐1β intracellularly. As shown by Northern blot analysis, Hg2+ inhibited the level of IL‐1β‐specific mRNA by 28% at 3.3 μM and completely at 33.3 μM. Only slight inhibitory effects were induced by Cu2+ at 33.3 μM. Interestingly, Ag+ at a concentration of 3.3 μM increased twofold the amount of IL‐1β‐specific mRNA. Our data show that IL‐1β production is altered at protein and mRNA levels by components released from fresh amalgam and by other heavy metal cations, suggesting a role of these cations in changes in the cell phenotype and IL‐1‐mediated cell functions. © 2000 John Wiley & Sons, Inc. J Biomed Mater Res, 51, 88–95, 2000. |
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ISSN: | 0021-9304 1097-4636 |
DOI: | 10.1002/(SICI)1097-4636(200007)51:1<88::AID-JBM12>3.0.CO;2-W |