Lithium Potentiates the FeCl2 Induced Free Radical Injury in Primary Mouse Cortical Cell Culture / 대한정신약물학회지
Korean Journal of Psychopharmacology
; : 468-474, 2006.
Article
em Ko
| WPRIM
| ID: wpr-163631
Biblioteca responsável:
WPRO
ABSTRACT
OBJECTIVES: For the past half century, lithium has been used for the acute and prophylactic treatment of bipolar disorder and recurrent depression. Recently, new pharmacological effects of Li+ have appeared, showing that Li+ can influence neuronal injury. We tested the effects of Li+ on free radical induced neuronal injury in primary murine cortical cell cultures. METHODS: Cortical cells were prepared from fetal mice (embryonic day 15) and exposed to 30 micrometer Fe2+ alone or with 5 mM Li+ or 5 mM Li+ alone for 24 hrs at Days in vitro (DIV) 14. Neuronal death was analyzed by measuring lactate dehydrogenase (LDH) release into media. The fluorescence of 2',7'-dichlorofluorescin (DCF) was measured in as a mean of estimating the formation of reactive oxygen species (ROS). RESULTS: Li+ alone does not produce neuronal injury itself but it potentiates Fe2+-induced neuronal injury through increasing the production of free radical. CONCLUSION: This study suggests that the effects of Li+ on neuronal survivorship may be injury type dependent and Li+ potentiate the free radical injury. Therefore in practice clinician should be cautious in using the lithium in the treatment of brain injured patients.
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Base de dados:
WPRIM
Assunto principal:
Transtorno Bipolar
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Encéfalo
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Taxa de Sobrevida
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Espécies Reativas de Oxigênio
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Técnicas de Cultura de Células
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Depressão
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Fluorescência
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L-Lactato Desidrogenase
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Lítio
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Necrose
Limite:
Animals
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Humans
Idioma:
Ko
Revista:
Korean Journal of Psychopharmacology
Ano de publicação:
2006
Tipo de documento:
Article