135 290

Cited 0 times in

3-nitropropionic Acid 투여 후 마우스 선조체에서 Apurinic/Apyrimidinic Endonuclease의 발현과 신경세포고사

Other Titles
 Expression of Apurinic/apyrimidinic Endonuclease and Neuronal Apoptosis in the Striatum after Treatment of 3-Nitropropionic Acid in Mice 
Authors
 조경주  ;  이두재  ;  이병인  ;  김경환 
Citation
 Journal of the Korean Neurological Association, Vol.23(4) : 510-518, 2005 
Journal Title
 Journal of the Korean Neurological Association 
ISSN
 1738-1428 
Issue Date
2005
MeSH
3-Nitropropionic acid ; Apurinic ; apyrimidinic endonuclese ; Reactive oxygen species ; Mananese tetrakis (40benzoic acid porphyrin) ; Reverse transcription polymerase chain reaction
Keywords
3-Nitropropionic acid ; Apurinic ; apyrimidinic endonuclese ; Reactive oxygen species ; Mananese tetrakis (40benzoic acid porphyrin) ; Reverse transcription polymerase chain reaction
Abstract
BACKGROUND: 3-Nitroporpionic acid (3-NP) is an irreVersible inhibitor of succinate dehydrogenase in mitochondria and can induce apoptosis-like cell death in the striatum. It has been reported that oxidative stress plays a role in the 3-NP induced neuronal damage. 3-NP induced striatal damage is implicated in the pathogenesis of several neurological diseases, such as chronic neurodegenerative diseases and stroke. The DNA repair enzyme, apurinic/apyrimidinic endonuclease (APE), is a multifunctional protein in the DNA base excision repair (BER) pathway. To clarify the relationship between APE and neuronal cell death associated with the apoptosis in the striatum was induced by 3-NP in vivo. METHODS: After intra-striatal injection of 3-NP, expression of the APE protein and mRNA were evaluated by Western blot, immunohistochemistry, RT-PCR and DNA fragmentation patterns. Oxidative DNA damage was investigated by detection of oxidized DNA, AP site and superoxide. RESULTS: Expression levels of APE was rapidly reduced as early as 1hr after injection of 3-NP. DNA fragmentation was observed 24 hours after 3-NP treatment but not 4 hours. APE gene expression was increased to 1hr after 3-NP treatment. The number of AP sites were reduced and the reduction of APE proteins were blocked by a superoxide scavenger, MnTBAP-treatment. CONCLUSIONS: These results suggest that the reduction of APE is the preceding event of DNA fragmentation that causes apoptosis and a decrease of APE may be induced by ROS after 3-NP treatment.
Files in This Item:
T200500405.pdf Download
DOI
OAK-2005-03351
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Lee, Byung In(이병인)
Cho, Kyuong Joo(조경주)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/147612
사서에게 알리기
  feedback

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse

Links