L-ASCORBIC ACID AND ARSENIC TRIOXIDE EXERT THE SYNERGISTIC EFFECT TO INDUCE THE GROWTH ARREST AND THE APOPTOSIS OF HUMAN ACUTE PROMYELOCYTIC LEUKEMIA, HL-60 VIA MODULATING REDOX STATUS, MAPK PATHWAY AND APOPTOSIS-RELATED FACTORS

  • Seong-Su Han (Samsung Medical Center, and Sungkyunkwan University School of Medicine) ;
  • Sook J. Lee (Samsung Medical Center, and Sungkyunkwan University School of Medicin) ;
  • Seung-Tae Chung (Department of Immunotoxicology, Korea Food and Drug Administratio) ;
  • Juno H. Eom (Department of Immunotoxicology, Korea Food and Drug Administratio) ;
  • Young-Joon Surh (College of Pharmacy, Seoul National University) ;
  • Hye K. Park (Samsung Medical Center, and Sungkyunkwan University School of Medicin) ;
  • Mary H. Park (Samsung Medical Center, and Sungkyunkwan University School of Medicin) ;
  • Won S. Kim (Samsung Medical Center, and Sungkyunkwan University School of Medicin) ;
  • Kihyun Kim (Samsung Medical Center, and Sungkyunkwan University School of Medicine)
  • Published : 2001.10.01

Abstract

There are increasing evidences that L-ascorbic acid (LAA) is selectively toxic to some types of tumors at physiological concentrations as a prooxidant, rather than antioxidant. However, the mechanism by which LAA initiates cellular signaling toward cell death is still unclear. Therefore, to determine whether LAA might be useful for the treatment of human acute promyelocytic leukemia (APL), HL-60 cells, the effects of LAA on proliferation, redox system, MAPK and induction of apoptotic cascades were investigated.(omitted)

Keywords