Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells.
- Author:
Yong sook KIM
1
;
Deok young JHON
;
Kee Young LEE
Author Information
1. Department of Food and Nutrition, College of Human Ecology, Chonnam National University, Gwangju 500-757, Korea.
- Publication Type:Original Article
- Keywords:
apoptosis;
Chang liver cell;
JNK1;
ROS;
selenite
- MeSH:
Acetylcysteine/pharmacology;
Anthracenes/pharmacology;
Apoptosis/*drug effects;
Catechin/*analogs & derivatives/pharmacology;
Cell Line;
DNA Fragmentation/*drug effects;
Free Radical Scavengers/pharmacology;
Humans;
Liver/cytology/*metabolism;
Mitogen-Activated Protein Kinase 8/antagonists & inhibitors/*metabolism;
Phosphorylation/drug effects;
Reactive Oxygen Species/*metabolism;
Selenium/*pharmacology;
Signal Transduction/drug effects
- From:Experimental & Molecular Medicine
2004;36(2):157-164
- CountryRepublic of Korea
- Language:English
-
Abstract:
Selenium is a dietary essential trace nutrient with important biological roles. Selenocompounds were reported to induce apoptosis in many types of tumor cells. In this study, we investigated the signaling pathway involved in the selenite-induced apoptosis using Chang liver cells as a non-malignant cell model. The Chang liver cell apoptosis induced by selenite (10 mM) was confirmed by DNA fragmentation and typical apoptotic nuclear changes. Treatment of selenite increased intracellular reactive oxygen species (ROS) level and c-Jun N-terminal kinase1 (JNK1) phosphorylation. The selenite-induced cell death was attenuated by SP600125, a specific inhibitor of JNK, and by dominant negative JNK1 (DN-JNK1). Antioxidants such as glutathione (GSH), N-acetyl cysteine (NAC), curcumin, epigallocatechin gallate (EGCG) and epicatechin (EC) inhibited selenite-induced intracellular ROS elevation and JNK1 phosphorylation. Our results suggest that selenite-induced apoptosis in Chang liver cells was preceded by the ROS generation and JNK1 activation.
