Korean J Psychopharmacol.  2006 Sep;17(5):468-474.

Lithium Potentiates the FeCl2 Induced Free Radical Injury in Primary Mouse Cortical Cell Culture

• Lee SH
• Lee YA
• Byun HY
• Gwag BJ
• Chung YK
• Noh JS

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.

Keyword

Lithium; Free radical injury; Necrosis

MeSH Terms

Animals
Bipolar Disorder
Brain
Cell Culture Techniques*
Depression
Fluorescence
Humans
L-Lactate Dehydrogenase
Lithium*
Mice*
Necrosis
Neurons
Reactive Oxygen Species
Survival Rate
L-Lactate Dehydrogenase
Lithium
Reactive Oxygen Species