Involvement of ROS and JNK1 in selenite-induced a poptosisin Chang liver cells
Experimental & Molecular Medicine
;
: 157-164, 2004.
Artigo
em Inglês
| 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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Fosforilação
/
Acetilcisteína
/
Selênio
/
Transdução de Sinais
/
Catequina
/
Linhagem Celular
/
Sequestradores de Radicais Livres
/
Espécies Reativas de Oxigênio
/
Apoptose
/
Proteína Quinase 8 Ativada por Mitógeno
Limite:
Humanos
Idioma:
Inglês
Revista:
Experimental & Molecular Medicine
Ano de publicação:
2004
Tipo de documento:
Artigo
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