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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2003.1
- 수록면
- 83 - 90 (8page)
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Arsenic trioxide (As2O3) has been found to be re-markably effective in the treatment of patients with acute promyelocytic leukemia (APL). Although evi-dences for the proapoptotic activity of As2O3 have been suggested in leukemic and other solid can-is far from clear. In the present study, we inves-tigated As2O3 affect on the stress-responsive sig-naling pathways and pretreatment with antioxidants using HepG2 cells. When treated with micromolar concentrations of As2O3, HepG2 cells became highly apoptotic paraleled with activation of cas-pase-3 and members of mitogen-activated protein kinases (MAPKs) including extracellular signal-re-gulated kinase (ERK) and c-jun NH2-terminal ki-nase (JNK) but not p38 MAP kinase. However, apoptosis by As2O3. Addition of n-acetyl cysteine (NAC) or diphenyleneiodonium (DPI) efectively pro-tected cells from apoptosis and significantly lo-wered As2O3-induced activation of caspase-3. How-ever, neither NAC nor DPI was able to efect ERK or JNK activation induced by As2O3. Guanidino-ethyldisulfide dihydrochloride (GED) and 2-ethyl- 2-thiopseudourea (ETU), known inhibitors of the inducible nitric oxide synthase (iNOS), also sup-pressed the apoptotic activity of As2O3. These re-sults suggest that As2O3 induces caspase-med-iated apoptosis involving a mechanism generating oxidative stres. However, activation of some stres- responsive signaling pathways by As2O3 may not be the major determinant in the course of apop-totic processes.
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