Long R C, Small W C, Brynes R K, Tidwell T, Goldstein J H, Vogler W R
Cancer Res. 1983 Feb;43(2):770-5.
Part of the cytotoxic action of alkyl-lysophospholipids (ALP) on leukemic cells is known to result from the lack of an O-alkyl cleavage enzyme and its antimetabolic effect which results in a toxic lysophospholipid buildup. Further, ALP (5 micrograms/ml) suppresses clonogenicity and tritiated thymidine uptake in HL60 cultures after 24 hr of exposure. The effect of ALP on two leukemic cell lines, HL60 and K562, measured by two nuclear magnetic resonance (NMR) techniques and examined by electron microscopy is reported. 31P-NMR spectroscopy indicates that the adenosine 5'-triphosphate:adenosine 5'-diphosphate ratios are unaffected after 24 hr, as is mitochondrial morphology, judging by electron micrographs. However, cell membrane integrity in HL60 is altered at that time. The earliest ALP effects occur in NMR internal water relaxation at 1 hr after ALP exposure, followed by a small reduction in tritiated thymidine uptake at 4 hr. No effect is observed in K562 cell cultures in morphology or NMR measurements. No new 31P-labeled metabolites were detected in either cell line as a result of drug treatment.
已知烷基溶血磷脂（ALP）对白血病细胞的部分细胞毒性作用源于缺乏O-烷基裂解酶及其抗代谢作用，这会导致有毒溶血磷脂的积累。此外，在暴露24小时后，ALP（5微克/毫升）会抑制HL60培养物中的克隆形成能力和氚标记胸腺嘧啶核苷摄取。本文报道了通过两种核磁共振（NMR）技术测量并通过电子显微镜检查的ALP对两种白血病细胞系HL60和K562的影响。31P-NMR光谱表明，24小时后三磷酸腺苷：二磷酸腺苷的比率未受影响，线粒体形态也是如此，这是根据电子显微镜照片判断的。然而，此时HL60中的细胞膜完整性发生了改变。ALP最早的作用发生在暴露1小时后的NMR内部水弛豫中，随后在4小时时氚标记胸腺嘧啶核苷摄取略有减少。在K562细胞培养物的形态或NMR测量中未观察到影响。药物处理后，在两种细胞系中均未检测到新的31P标记代谢物。
