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Effect of homocysteine on survival of human glial cells
H. Škovierová, S. Mahmood, E. Blahovcová, J. Hatok, J. Lehotský, R. Murín
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- buněčná smrt účinky léků fyziologie MeSH
- homocystein farmakologie MeSH
- kultivované buňky MeSH
- lidé MeSH
- nádorové buněčné linie MeSH
- neuroglie účinky léků fyziologie MeSH
- neurony účinky léků fyziologie MeSH
- viabilita buněk účinky léků fyziologie MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Several neurodegenerative conditions, such as Alzheimer's disease and Parkinson's disease, or vascular dementia and cognitive impairment, are associated with mild hyperhomocysteinemia. Hyperhomocysteinemia is defined as an increase of the homocysteine (Hcy) level beyond 10 microM. Although the adverse effect of Hcy on neurons is well documented, knowledge about the impact of this amino acid on glial cells is missing. Therefore, with the aim to evaluate the neurotoxic properties of Hcy on glial cells, we used a glioblastoma cell line as a study model. The viability of cells was assayed biochemically and cytologically. At a concentration around 50 microM in the culture medium D,L-Hcy induced cell death. It is noteworthy that Hcy induces cell death of human glial cells at concentrations encountered during mild hyperhomocysteinemia. Therefore, we propose that Hcy-induced impairment of neuronal functions along with damage of glial cells may contribute to the etiopathogenesis of neurodegenerative diseases associated with hyperhomocysteinemia.
Citace poskytuje Crossref.org
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- $a Several neurodegenerative conditions, such as Alzheimer's disease and Parkinson's disease, or vascular dementia and cognitive impairment, are associated with mild hyperhomocysteinemia. Hyperhomocysteinemia is defined as an increase of the homocysteine (Hcy) level beyond 10 microM. Although the adverse effect of Hcy on neurons is well documented, knowledge about the impact of this amino acid on glial cells is missing. Therefore, with the aim to evaluate the neurotoxic properties of Hcy on glial cells, we used a glioblastoma cell line as a study model. The viability of cells was assayed biochemically and cytologically. At a concentration around 50 microM in the culture medium D,L-Hcy induced cell death. It is noteworthy that Hcy induces cell death of human glial cells at concentrations encountered during mild hyperhomocysteinemia. Therefore, we propose that Hcy-induced impairment of neuronal functions along with damage of glial cells may contribute to the etiopathogenesis of neurodegenerative diseases associated with hyperhomocysteinemia.
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