Takeuchi T, Nakajima M, Morimoto K
Department of Hygiene and Preventive Medicine, Osaka University School of Medicine, Japan.
Biochem Biophys Res Commun. 1994 Dec 30;205(3):1803-7. doi: 10.1006/bbrc.1994.2879.
Calyculin A(CA) induced 8-hydroxydeoxyguanosine (8OHdG), typical of mutagenic oxidative DNA damage, in N-Formyl-Methionyl-Leucyl-Phenylalanine (FMLP)-stimulated dimethyl sulfoxide(DMSO)-differentiated HL60(DMSO-HL60), which has characteristics similar to those of human neutrophils. CA enhanced O2-generation in FMLP-stimulated DMSO-HL60. CA by itself neither induced 8OHdG nor O2-generation. FMLP by itself induced O2-generation, however, it did not induce 8OHdG. These findings suggest that CA exerts its tumor promotion activity through modulating O2-generation and through inducing oxidative DNA damage and that a common bioactive peptide induces oxidative DNA damage under a certain condition.
在经N-甲酰甲硫氨酰亮氨酰苯丙氨酸(FMLP)刺激的二甲基亚砜(DMSO)分化的HL60(DMSO-HL60)细胞中,花萼海绵诱癌素A(CA)诱导产生了具有诱变氧化DNA损伤典型特征的8-羟基脱氧鸟苷(8OHdG),DMSO-HL60细胞具有与人类中性粒细胞相似的特征。CA增强了FMLP刺激的DMSO-HL60细胞中的超氧阴离子(O₂)生成。CA自身既不诱导8OHdG产生,也不诱导O₂生成。FMLP自身可诱导O₂生成,然而,它不诱导8OHdG产生。这些发现表明,CA通过调节O₂生成和诱导氧化DNA损伤来发挥其肿瘤促进活性,并且一种常见的生物活性肽在特定条件下可诱导氧化DNA损伤。