Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Biomaterials. 2003 Mar;24(6):981-7.

Mercuric chloride: toxicity and apoptosis in a human oligodendroglial cell line MO3.13.

Author information

  • 1Turner Dental School, The University of Manchester, Manchester, UK.

Abstract

A human-human oligodendroglial cell line MO3.13 was chosen in this study to model the loss of oligodendrocytes that occurs during episodes of multiple sclerosis. The influence of mercuric chloride (HgCl(2)) upon cell viability specifically the mode of cell death, whether by an active apoptotic mechanism or passive necrosis was determined by morphological and biochemical analysis. Mitochondrial dehydrogenase activity MTT assay showed that HgCl(2) had toxic effects on MO3.13 cells at levels of (5-25 microM) with approximately 50% cell death observed at 58 microM. Death of cells was dependent on both time and concentrations of HgCl(2). Differentiated MO3.13 cells exposed to low concentrations (25 microM) of HgCl(2) exhibited features of apoptotic cell death, including cell shrinkage and chromatin condensation. High doses of HgCl(2) (>100 microM) induced death with characteristics of necrosis. Biochemical analysis showed that HgCl(2) activated the caspase family of proteases. This was measured directly by cleavage of fluorescent substrates and by immunoblotting assay of caspase substrate proteins; alpha-fodrin, lamin B and poly (ADP-ribose) polymerase (PARP). These results indicate that HgCl(2) is toxic at low concentrations for oligodendroglial cells and that the MO3.13 cell line dies in an apoptotic manner when exposed to low concentrations of HgCl(2). However, blood mercury concentrations in vivo in a normal population with amalgam restorations are lower by a factor of some 500 times than those causing toxicity in vitro suggesting a good safety margin in respect of environmental uptake.

PMID:
12504520
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk