title: Induction of the differentiation of HL-60 promyelocytic leukemia cells by L-ascorbic acid.
abstract: The present study was undertaken to examine the effect of L-ascorbic acid (LAA) on the growth of HL-60 promyelocytic leukemia cells, besides induction of apoptosis. LAA (> or = 10(-4) M) was found to markedly inhibit the proliferation of HL-60 in liquid culture and clonogenicity in semisolid culture. Moreover, LAA-treated HL-60 showed activity to produce chemiluminescence and expressed CD 66b cell surface antigens, indicating that LAA induces the differentiation of HL-60 mainly into granulocytes. The results are supported by morphological changes of LAA-treated HL-60 into segmented neutrophils. Therefore, the inhibitory effect of LAA on the growth of HL-60 cells seems to arise from the induction of differentiation. To assess the potential role of LAA, cells were exposed to oxygen radical scavengers in the absence or presence of LAA. Catalase abolished and superoxide dismutase promoted LAA-induced differentiation of HL-60. Thus, H2O2 produced as a result of LAA treatment seems to play a major role in induction of HL-60 differentiation.
authors.affiliation: Department of Pharmacology, College of Medicine, Cheju National University, Ara 1-dong, Jeju 690-756, Korea.
authors.forename: Hee Kyoung
authors.initials: HK
authors.lastname: Kang
authors.forename: Jung Han
authors.initials: JH
authors.lastname: Suh
authors.forename: Jung Jin
authors.initials: JJ
authors.lastname: Lee
authors.forename: Sun Hee
authors.initials: SH
authors.lastname: Yoon
authors.forename: Jin Won
authors.initials: JW
authors.lastname: Hyun
authors.forename: Seong Won
authors.initials: SW
authors.lastname: Choi
authors.forename: Jeong Yun
authors.initials: JY
authors.lastname: Choi
authors.forename: Kyung Ha
authors.initials: KH
authors.lastname: Ryu
authors.forename: Myung Hee
authors.initials: MH
authors.lastname: Chung
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis; D015214:Antigens, Differentiation, Myelomonocytic / Q000096:biosynthesis; D000951:Antigens, Neoplasm / Q000096:biosynthesis; D017209:Apoptosis; D001205:Ascorbic Acid / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002454:Cell Differentiation / Q000187:drug effects*; D002455:Cell Division; D004305:Dose-Response Relationship, Drug; D006098:Granulocytes / Q000378:metabolism; D018922:HL-60 Cells; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008163:Luminescent Measurements; D063268:Sialic Acid Binding Ig-like Lectin 3; D013482:Superoxide Dismutase / Q000378:metabolism; D013997:Time Factors
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D000951:Antigens, Neoplasm; C571163:CD33 protein, human; D015815:Cell Adhesion Molecules; D063268:Sialic Acid Binding Ig-like Lectin 3; D006861:Hydrogen Peroxide; D002374:Catalase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid