Journal of Environmental Pathology, Toxicology and Oncology

ISSN for PRINT: 0731-8898

For Online Access

Best Paper Award Selection - Editorial Board Site

2002, Volume21

Issue 2

124 pages

Issue price - $160.00

Yong Soo Lee
Department of Physiology, College of Medicine, Kwan-dong University, Kangnung, Korea

Eun Jin Kwon
College of Pharmacy, Yeungnam University, Kyongsan, Korea

Da Qing Jin
College of Pharmacy, Yeungnam University, Kyongsan, Korea

Seung Hee Park
College of Pharmacy, Yeungnam University, Kyongsan, Korea

Young Shin Kang
Department of Physiology, College of Medicine, Kwan-dong University, Kangnung, Korea

Keun Huh
College of Pharmacy, Yeungnam University, Kyongsan, Korea

Jung-Ae Kim
College of Pharmacy, Yeungnam University, Dae-Dong 214-1, Kyongsan 712-749, Korea

Cyclooxygenases (COX) appear to be involved in the mechanism of apoptosis in various cancer cells. In this study we investigated the role of COX in the capsaicin (Cap)-induced apoptosis in SK-N-SH human neuroblastoma cells. Cap induced decreased cell viability and apoptosis in a dose-dependent manner. Cap also significantly reduced the basal generation of reactive oxygen species (ROS) and lipid peroxidation in a time-dependent fashion. Cap markedly suppressed the expression of COX-1 and COX-2. Pretreatment with NS-398, a selective COX-2 inhibitor, or indomethacin, a nonselective COX inhibitor, significantly enhanced the Cap-induced decreased cell viability and apoptosis. Exogenous application of an oxidant, Н₂О₂, significantly prevented the Cap-induced apoptosis and suppressed the expression of COX isoforms. These results suggest that redox status-dependent regulation of COX expression may mediate apoptosis induced by Cap in human neuroblastoma cells.

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