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

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Title: Mercuric chloride: toxicity and apoptosis in a human oligodendroglial cell line MO3.13
Authors: Issa, Y.1, Watts, D.C.1, Duxbury, A.J.1 john.duxbury@man.ac.uk, Brunton, P.A.1, Watson, M.B.2, Waters, C.M.2
Source: Biomaterials. Mar2003, Vol. 24 Issue 6, p981. 7p.
Subjects: Multiple sclerosis, Mercuric chloride, Nervous system, Apoptosis
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 (HgCl2) 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 HgCl2 had toxic effects on MO3.13 cells at levels of (5–25 μm) with approximately 50% cell death observed at 58 μm. Death of cells was dependent on both time and concentrations of HgCl2. Differentiated MO3.13 cells exposed to low concentrations (25 μm) of HgCl2 exhibited features of apoptotic cell death, including cell shrinkage and chromatin condensation. High doses of HgCl2 (>100 μm) induced death with characteristics of necrosis. Biochemical analysis showed that HgCl2 activated the caspase family of proteases. This was measured directly by cleavage of fluorescent substrates and by immunoblotting assay of caspase substrate proteins; α-fodrin, lamin B and poly (ADP-ribose) polymerase (PARP). These results indicate that HgCl2 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 HgCl2. 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. [Copyright &y& Elsevier]
Copyright of Biomaterials is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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DbLabel: Engineering Source
An: 8722751
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  Data: Mercuric chloride: toxicity and apoptosis in a human oligodendroglial cell line MO3.13
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  Data: <searchLink fieldCode="JN" term="%22Biomaterials%22">Biomaterials</searchLink>. Mar2003, Vol. 24 Issue 6, p981. 7p.
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  Data: <searchLink fieldCode="DE" term="%22Multiple+sclerosis%22">Multiple sclerosis</searchLink><br /><searchLink fieldCode="DE" term="%22Mercuric+chloride%22">Mercuric chloride</searchLink><br /><searchLink fieldCode="DE" term="%22Nervous+system%22">Nervous system</searchLink><br /><searchLink fieldCode="DE" term="%22Apoptosis%22">Apoptosis</searchLink>
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  Data: 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 (HgCl2) 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 HgCl2 had toxic effects on MO3.13 cells at levels of (5–25 μm) with approximately 50% cell death observed at 58 μm. Death of cells was dependent on both time and concentrations of HgCl2. Differentiated MO3.13 cells exposed to low concentrations (25 μm) of HgCl2 exhibited features of apoptotic cell death, including cell shrinkage and chromatin condensation. High doses of HgCl2 (>100 μm) induced death with characteristics of necrosis. Biochemical analysis showed that HgCl2 activated the caspase family of proteases. This was measured directly by cleavage of fluorescent substrates and by immunoblotting assay of caspase substrate proteins; α-fodrin, lamin B and poly (ADP-ribose) polymerase (PARP). These results indicate that HgCl2 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 HgCl2. 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. [Copyright &y& Elsevier]
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  Data: <i>Copyright of Biomaterials is the property of Elsevier B.V. and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1016/S0142-9612(02)00436-2
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        Text: English
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        Type: general
      – SubjectFull: Mercuric chloride
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      – SubjectFull: Nervous system
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      – SubjectFull: Apoptosis
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              Text: Mar2003
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              Y: 2003
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