Exp Mol Med.  2004 Apr;36(2):157-164.

Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells

• Kim YS
• Jhon DY
• Lee KY

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.

Keyword

apoptosis; Chang liver cell; JNK1; ROS; selenite

MeSH Terms

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