Hoggard P G, Kewn S, Barry M G, Khoo S H, Back D J
Department of Pharmacology & Therapeutics, University of Liverpool, United Kingdom.
Antimicrob Agents Chemother. 1997 Jun;41(6):1231-6. doi: 10.1128/AAC.41.6.1231.
Drugs commonly administered to patients infected with the human immunodeficiency virus (HIV) have been studied for their propensity to alter the intracellular phosphorylation of the anti-HIV nucleoside analog stavudine (2',3'-dideoxy-2',3'-didehydrothymidine; d4T) in peripheral blood mononuclear cells (PBMCs) and U937 cells in vitro. PBMCs isolated from the blood of healthy volunteers were stimulated by the mitogen phytohemagglutinin (10 microg/ml) for 72 h. Stimulated PBMCs (3 x 10(6) cells/plate) were then incubated with [3H]d4T (0.65 microCi; 3 microM) and either acyclovir, dapsone, ddC, ddI, fluconazole, foscarnet, ganciclovir, itraconazole, lobucavir, ranitidine, ribavirin, rifampin, sorivudine, sulfamethoxazole, trimethoprim, lamivudine (3TC), zidovudine, or thymidine (30 and 300 microM) for 24 h. Doxorubicin and drugs showing some evidence of inhibition were also studied at 0.3 and 3 microM. Cells were extracted overnight with 60% methanol prior to analysis by radiometric high-performance liquid chromatography. Additional data for nine of the drugs were obtained by incubation with [3H]d4T in U937 cells for 24 h. The effect of d4T (0.2 to 20 microM) on zidovudine (0.65 microCi; 0.018 microCi) phosphorylation was also studied. Zidovudine significantly reduced d4T total phosphates in PBMCs and U937 cells (in PBMCs to 33% [P < 0.001] and 17% [P < 0.001] of that in control cells at 3 and 30 microM, respectively). A small reduction in zidovudine phosphorylation was seen with d4T but only at d4T:zidovudine ratios of 100 and 1,000. Of the other compounds screened, only thymidine, ribavirin, and doxorubicin produced inhibition of d4T phosphorylation in both PBMCs and U937 cells. However, doxorubicin was cytotoxic at 3 microM. The decrease in d4T phosphorylation in the presence of ribavirin is consistent with previous findings with zidovudine. Although ddC significantly inhibited the phosphorylation of d4T in PBMCs, this was not seen in U937 cells, and it is probable that the findings in PBMCs are related to mitochondrial toxicity [based on 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide cytotoxicity assay]. The only drugs screened which may interfere with d4T phosphorylation at clinically relevant concentrations were zidovudine, ribavirin, and doxorubicin.
已对常用于感染人类免疫缺陷病毒(HIV)患者的药物进行了研究,观察其在体外对人外周血单核细胞(PBMC)和U937细胞中抗HIV核苷类似物司他夫定(2',3'-二脱氧-2',3'-二脱氢胸苷;d4T)细胞内磷酸化的影响倾向。从健康志愿者血液中分离的PBMC用丝裂原植物血凝素(10μg/ml)刺激72小时。然后将刺激后的PBMC(3×10⁶细胞/孔)与[³H]d4T(0.65μCi;3μM)以及阿昔洛韦、氨苯砜、双脱氧胞苷(ddC)、双脱氧肌苷(ddI)、氟康唑、膦甲酸、更昔洛韦、伊曲康唑、洛布卡韦、雷尼替丁、利巴韦林、利福平、索立夫定、磺胺甲恶唑、甲氧苄啶、拉米夫定(3TC)、齐多夫定或胸腺嘧啶(30和300μM)孵育24小时。还研究了阿霉素以及显示出一定抑制证据的药物在0.3和3μM浓度下的情况。在通过放射性高效液相色谱分析之前,细胞用60%甲醇提取过夜。通过在U937细胞中与[³H]d4T孵育24小时获得了其中九种药物的其他数据。还研究了d4T(0.2至20μM)对齐多夫定(0.65μCi;0.018μCi)磷酸化的影响。齐多夫定显著降低了PBMC和U937细胞中d4T的总磷酸盐含量(在PBMC中,在3μM和30μM时分别降至对照细胞的33%[P<0.001]和17%[P<0.001])。d4T使齐多夫定磷酸化略有降低,但仅在d4T:齐多夫定比例为100和1000时出现。在所筛选的其他化合物中,只有胸腺嘧啶、利巴韦林和阿霉素在PBMC和U937细胞中均抑制d4T磷酸化。然而,阿霉素在3μM时具有细胞毒性。利巴韦林存在时d4T磷酸化的降低与先前关于齐多夫定的研究结果一致。虽然ddC在PBMC中显著抑制d4T的磷酸化,但在U937细胞中未观察到,PBMC中的这一结果可能与线粒体毒性有关[基于3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐细胞毒性试验]。在临床相关浓度下可能干扰d4T磷酸化的所筛选药物只有齐多夫定、利巴韦林和阿霉素。