Hrabák András, Csuka Ildikó, Bajor Tamás, Csatáry László K
Department of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, VIII, Puskin u. 9, P.O. Box 260, H-1444 Budapest, Hungary.
Cancer Lett. 2006 Jan 18;231(2):279-89. doi: 10.1016/j.canlet.2005.02.008.
Rat peritoneal macrophages were induced to produce high amounts of nitric oxide (NO) when rats were challenged by MTH68/H, (a live attenuated oncolytic Newcastle disease virus strain). The increase in NO production was observed to be viral particle dose dependent. The higher NO production measured could be due to the enhanced expression of NO synthase II enzyme. In addition, viral administration caused a higher macrophage cell count in the peritoneal cavity of treated rats. Interleukin-1 and granulocyte-monocyte colony stimulating factors were also produced by the induced macrophages. COS 7, a transformed cell line was killed by both NO donors and activated macrophages; the latter effect was markedly decreased in the presence of the inhibitors of NO production. Cytotoxic effect of NO was evidenced by the decrease of cell viability and proliferation of COS 7 cells. Excessive NO production may also be cytotoxic for macrophages themselves as proved by the addition of exogenous NO donors. These results strongly suggested the participation of induced NO synthesis of macrophages in the anti-tumor effect of MTH-68/H vaccine treatment.
当大鼠受到MTH68/H(一种减毒活溶瘤新城疫病毒株)攻击时,大鼠腹腔巨噬细胞被诱导产生大量一氧化氮(NO)。观察到NO产量的增加呈病毒颗粒剂量依赖性。测得的较高NO产量可能归因于一氧化氮合酶II酶表达的增强。此外,病毒给药导致治疗大鼠腹腔内巨噬细胞数量增加。诱导的巨噬细胞还产生白细胞介素-1和粒细胞-单核细胞集落刺激因子。COS 7,一种转化细胞系,被NO供体和活化的巨噬细胞杀死;在存在NO产生抑制剂的情况下,后一种效应明显降低。COS 7细胞活力和增殖的降低证明了NO的细胞毒性作用。如添加外源性NO供体所证明的,过量的NO产生对巨噬细胞自身也可能具有细胞毒性。这些结果强烈表明,诱导巨噬细胞合成NO参与了MTH-68/H疫苗治疗的抗肿瘤作用。