Esteves-Souza Andressa, Lucio Kelly Araújo, Da Cunha Andréa Sousa, Da Cunha Pinto Angelo, Da Silva Lima Edson Luiz, Camara Celso Amorim, Vargas Maria Domingues, Gattass Cerli Rocha
Instituto de Biofísica Carlos Chagas Filho, CCS, Universidade Federal do Rio de Janeiro, 21949-900 Rio de Janeiro, Brazil.
Oncol Rep. 2008 Jul;20(1):225-31.
Polyamine-naphthoquinone conjugates 5a-c were synthesized by nucleophilic displacement of 2-methoxy-lawsone 3a, 2-methoxylapachol 3b and 2-methoxy-nor-lapachol 3c with the polyamine N1-Boc-N5-Bn-spermidine 4. Unprotected derivatives 6a-c were synthesized to evaluate the effect of the protective Boc group on the activity of compounds 5a-c. The colorimetric MTT assay was used to evaluate their cytotoxic activity. All compounds were active against human lines of promyelocytic leukemia (HL-60), lung cancer (GLC4), Burkitt lymphoma (Daudi) and a mouse breast tumor (Ehrlich carcinoma), but only unprotected 6a-c showed activity against the human line of melanoma (MV-3). IC50 values were obtained from dose response curves by linear regression. DNA fragmentation was measured by quantification of the subG1 peak of the cell cycle. Apoptosis of HL-60 treated with 5c was dose-dependent. The amount of DNA fragmentation observed by exposure of HL-60 to 25 microM of compounds 5a-c and 6a-c is compatible with the decrease in viability induced by the drugs at this concentration. Production of ROS was measured by H2-CFDA. Kinetics of HL-60 DNA fragmentation and ROS formation by 5c indicated that production of ROS precedes cell death. In conclusion, spermidine-1,4-naphthoquinone conjugates exhibited an increase in activity compared with the natural products and induced apoptosis of tumor cell lines by a mechanism that is mediated, at least in part, by ROS production.
通过2-甲氧基胡桃醌3a、2-甲氧基拉帕醇3b和2-甲氧基-去甲拉帕醇3c与多胺N1-Boc-N5-Bn-亚精胺4的亲核取代反应合成了多胺-萘醌共轭物5a-c。合成了未受保护的衍生物6a-c,以评估保护基团Boc对化合物5a-c活性的影响。采用比色法MTT试验评估其细胞毒性活性。所有化合物对人早幼粒细胞白血病细胞系(HL-60)、肺癌细胞系(GLC4)、伯基特淋巴瘤细胞系(Daudi)和小鼠乳腺肿瘤细胞系(艾氏癌)均有活性,但只有未受保护的6a-c对人黑色素瘤细胞系(MV-3)有活性。通过线性回归从剂量反应曲线获得IC50值。通过定量细胞周期的亚G1峰来测量DNA片段化。用5c处理的HL-60细胞凋亡呈剂量依赖性。将HL-60暴露于25 microM的化合物5a-c和6a-c时观察到的DNA片段化量与该浓度下药物诱导的活力降低相一致。通过H2-CFDA测量活性氧(ROS)的产生。5c诱导HL-60细胞DNA片段化和ROS形成的动力学表明,ROS的产生先于细胞死亡。总之,与天然产物相比,亚精胺-1,4-萘醌共轭物的活性有所增加,并通过至少部分由ROS产生介导的机制诱导肿瘤细胞系凋亡。