Geurtsen W, Zahn R K, Maidhof A, Müller W E
Gan. 1981 Apr;72(2):259-63.
Neocarzinostatin (NCS), which causes DNA strand scission both in vitro and in vivo, reversibly inhibits the growth of both unpermeabilized and lysolecithin-permeabilized P815 mast cells (mouse leukemic cells). Kinetic experiments with NCS-pretreated cells revealed that the permeabilized cells are more strongly affected than the unpermeabilized cells, indicating that the membrane protects the cells against the influence of NCS. The two major DNA polymerase activities (form alpha and form beta) were determined in permeabilized cells during the lag phase of growth, after NCS treatment, and an 8.5-fold higher DNA polymerase beta activity was observed in NCS-treated cells than in controls. The activity of the second enzyme, DNA polymerase alpha, was low during the period of cell proliferation.
新制癌菌素（NCS）在体外和体内均可引起DNA链断裂，它能可逆地抑制未通透化和溶血卵磷脂通透化的P815肥大细胞（小鼠白血病细胞）的生长。对经NCS预处理的细胞进行的动力学实验表明，通透化细胞比未通透化细胞受影响的程度更大，这表明细胞膜可保护细胞免受NCS的影响。在生长延迟期、NCS处理后，对通透化细胞中的两种主要DNA聚合酶活性（α型和β型）进行了测定，结果发现，经NCS处理的细胞中DNA聚合酶β的活性比对照细胞高8.5倍。在细胞增殖期间，第二种酶即DNA聚合酶α的活性较低。
