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Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells
Experimental & Molecular Medicine ; : 157-164, 2004.
Article in English | WPRIM | ID: wpr-37853
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.
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Full text: Available Index: WPRIM (Western Pacific) Main subject: Phosphorylation / Acetylcysteine / Selenium / Signal Transduction / Catechin / Cell Line / Free Radical Scavengers / Reactive Oxygen Species / Apoptosis / Mitogen-Activated Protein Kinase 8 Limits: Humans Language: English Journal: Experimental & Molecular Medicine Year: 2004 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Phosphorylation / Acetylcysteine / Selenium / Signal Transduction / Catechin / Cell Line / Free Radical Scavengers / Reactive Oxygen Species / Apoptosis / Mitogen-Activated Protein Kinase 8 Limits: Humans Language: English Journal: Experimental & Molecular Medicine Year: 2004 Type: Article