Shambaugh G E, Blumenschein G R
Infect Immun. 1974 Feb;9(2):384-90. doi: 10.1128/iai.9.2.384-390.1974.
Three mitogenic agents, phytohemagglutinin (PHA), staphylococcal enterotoxin B (SEB), and concanavalin A (Con A) were tested for their effects on deoxyribonucleic acid (DNA) synthesis in the normal human lymphocyte. When optimal concentrations of PHA and SEB were combined, tritiated thymidine incorporation in lymphocytes derived from several donors was enhanced significantly. In the presence of graded concentrations of one of these mitogens added to fixed optimal concentrations of the other, this enhancement was shown to be additive. By contrast, when PHA or SEB were combined with Con A, the resulting thymidine incorporation was slightly lower than for either mitogen alone. An inhibition of further thymidine incorporation when puromycin was added to lymphocytes incubated with PHA and SEB suggested that the additive effect of these mitogens was due to increased enzyme synthesis. To define potential differences in mechanisms of action underlying the additive effect of SEB and PHA, the relative contribution of the de novo and salvage pathways for pyrimidine biosynthesis was tested with cytidine, a specific salvage pathway inhibitor. Cytidine (10(-3) M) inhibited synthesis through the salvage pathway, but did not significantly alter induction of carbamyl phosphate synthetase II, the rate-limiting enzyme for the de novo pathway. An inhibition of DNA synthesis by millimolar cytidine concentrations in lymphocytes incubated with PHA or SEB, singly or in combination, suggested that pyrimidines for the observed enhancement of DNA synthesis were derived largely via the salvage pathway.
对三种促有丝分裂剂,即植物血凝素(PHA)、葡萄球菌肠毒素B(SEB)和刀豆球蛋白A(Con A)对正常人淋巴细胞中脱氧核糖核酸(DNA)合成的影响进行了测试。当PHA和SEB的最佳浓度联合使用时,来自多个供体的淋巴细胞中氚标记胸腺嘧啶核苷的掺入显著增强。在将这些促有丝分裂剂之一的分级浓度添加到另一种的固定最佳浓度存在下,这种增强显示为相加性。相比之下,当PHA或SEB与Con A联合使用时,产生的胸腺嘧啶核苷掺入略低于单独使用任何一种促有丝分裂剂的情况。当将嘌呤霉素添加到用PHA和SEB孵育的淋巴细胞中时,对进一步的胸腺嘧啶核苷掺入的抑制表明这些促有丝分裂剂的相加作用是由于酶合成增加。为了确定SEB和PHA相加作用背后潜在的作用机制差异,用胞苷(一种特异性补救途径抑制剂)测试了嘧啶生物合成的从头合成途径和补救途径的相对贡献。胞苷(10⁻³ M)抑制了通过补救途径的合成,但没有显著改变氨甲酰磷酸合成酶II(从头合成途径的限速酶)的诱导。在单独或联合使用PHA或SEB孵育的淋巴细胞中,毫摩尔浓度的胞苷对DNA合成的抑制表明,观察到的DNA合成增强所需的嘧啶很大程度上是通过补救途径获得的。