Lithium Potentiates the FeCl2 Induced Free Radical Injury in Primary Mouse Cortical Cell Culture.
- Author:
Seung Hye LEE
1
;
Young Ae LEE
;
Han Yeol BYUN
;
Byoung Joo GWAG
;
Young Ki CHUNG
;
Jai Sung NOH
Author Information
1. Department of Psychiatry, 3Pharmacology, Ajou University, School of Medicine, Suwon, Korea. jsnoh@ajou.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
Lithium;
Free radical injury;
Necrosis
- MeSH:
Animals;
Bipolar Disorder;
Brain;
Cell Culture Techniques*;
Depression;
Fluorescence;
Humans;
L-Lactate Dehydrogenase;
Lithium*;
Mice*;
Necrosis;
Neurons;
Reactive Oxygen Species;
Survival Rate
- From:Korean Journal of Psychopharmacology
2006;17(5):468-474
- CountryRepublic of Korea
- Language:Korean
-
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.
