Caspase is Regulated by ROS in CT Induced Neuronal Cell Death.
- Author:
Hee Sun CHAE
1
;
Yoo Hun SUH
;
Kyung Yong KIM
;
Won Bok LEE
;
Sung Su KIM
Author Information
1. Department of Anatomy, College of Medicine, Chung-Ang University, Seoul, Korea. sungsu@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Alzheimer's disease;
Neuronal cell death;
Reactive oxygen speces;
Caspase;
Amyloid
- MeSH:
Alzheimer Disease;
Amyloid;
Caspase 3;
Cell Death*;
Negotiating;
Neurons*;
Reactive Oxygen Species
- From:Korean Journal of Anatomy
2003;36(2):133-140
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Carboxy-terminal fragment of amyloid precusor protein (CT) is a candidate of causal molecule in the pathogenesis of Alzheimer's disease. Although it has been identified that CT shows cytotoxicity in various types of cells, little is known about the molecular mechanism of the cytotoxic on neuronal cells by CT. In the present study, we investigated the relevance of reactive oxygen species (ROS) generation to CT induced cell death in SK-N-SH cells. We showed CT induced ROS production and antioxidant GSH inhibited the increase of ROS production, thereby preventing neuronal cell death. These results indicate that CT induce neuronal cell death through mediation of ROS. Furthermore, increase of caspase activity resulted from CT reduced by GSH. It is implicate that caspase-3 may act downstream of ROS in the pathway neuronal cell death induced by CT.
