Polatnick J, Arlinghaus R B
J Virol. 1967 Dec;1(6):1130-4. doi: 10.1128/JVI.1.6.1130-1134.1967.
Actinomycin D, at a concentration that inhibits cellular ribonucleic acid (RNA) synthesis, inhibited the production of foot-and-mouth disease virus-induced RNA polymerase in baby hamster kidney cells. Inhibition was proportional to exposure time and reached 85% when actinomycin D was added 90 min before infection. Polymerase production was inhibited to the same extent in growth and minimal media, and the kinetics of its appearance were slightly different than in untreated cells. Enzyme preparations from actinomycin-treated cells having one-third to one-tenth the activity of untreated samples gave products with RNA profiles similar to those of controls. The 37S viral peak, 20S ribonuclease-resistant peak, and 26 to 28S peaks were present in all cases. Actinomycin D did not consistently inhibit virus production in either medium. Insulin did not prevent the actinomycin induced inhibition of polymerase and virus production from occurring.
放线菌素D在抑制细胞核糖核酸（RNA）合成的浓度下，可抑制幼仓鼠肾细胞中口蹄疫病毒诱导的RNA聚合酶的产生。抑制作用与暴露时间成正比，在感染前90分钟添加放线菌素D时，抑制率达到85%。在生长培养基和基本培养基中，聚合酶的产生受到同等程度的抑制，其出现的动力学与未处理细胞略有不同。来自经放线菌素处理的细胞的酶制剂，其活性为未处理样品的三分之一至十分之一，产生的RNA谱与对照相似。在所有情况下均存在37S病毒峰、20S抗核糖核酸酶峰以及26至28S峰。放线菌素D在两种培养基中均未始终如一地抑制病毒产生。胰岛素不能阻止放线菌素诱导的聚合酶抑制和病毒产生。
