Expression and function of apoptosis-regulatory genes induced by oxidative stress in human neuroblastoms cells = Human neuroblastoma cell에서 oxidative stress에 의한 apoptosis 조절유전자의 발현과 기능

다국어 초록 (Multilingual Abstract)

Apoptosis has been implicated in the pathophysiological mechanisms of various neurodegenerative diseases. In a variety of cell types oxidative stress has been demonstrated to play an important role in the apoptotic cell death.
However, the exact mechanism of oxidative stress-induced apoptosis in neuronal cells is not known. In this study we induced oxidative stress in IMR-32 human neuroblastoma cells with tert-butylhydroperoxide (TBHP), which was confirmed by significantly reduced glutathione content and glutathione reductase activity, and increased glutathione peroxidase activity. TBHP induced decreased cell viability and increased DNA fragmentation, a hallmark of apoptosis, in a dose-dependent manner. TBHP also induced a sustained increase in intracellular Ca^2+ concentration, which was completely prevented either by EGTA, an extracellular Ca^2+ chelator or by flufenamic acid (FA), a non-selective cation channel (NSCC) blocker. These results indicate that the TBHP-induced intracellular Ca^2+ increase may be due to Ca^2+ influx through the activation of NSCCs. In addition, treatment with either an intracellular Ca^2+ chelator (BAPTA/AM) or FA significantly suppressed the TBHP-induced apoptosis.
Moreover, TBHP increased the expression of p53 gene, but decreased c-myc gene expression. Taken together, these results suggest that the oxidative stress-induced apoptosis in neuronal cells may be mediated through the activation of intracellular Ca^2+ signals and altered expression of p53 and c myc.

목차 (Table of Contents)

• ABSTRACT
• 1.INTRODCUTION
• 2.DISCUSSION
• REFERENECES