Khramtsova S N, Potapova G I, Dmitrieva L V, Shapot V S
Biokhimiia. 1986 Apr;51(4):635-43.
Biochemical impairments in spleen immunocompetent cells (T- and B-lymphocytes) were revealed in host (C3HA mice) of transplantable and ortoaminoazotoluol-induced hepatomas in the course of their growth. As soon as hepatoma emerged (chemical carcinogenesis), the activity of adenosine deaminase and purine nucleoside phosphorylase in T- and B-lymphocytes were found to be reduced 2-6 and 7-10-fold, respectively in parallel with the impairment of their immune system. These alterations were accompanied by the increase in concentrations of dGTP in T-lymphocytes (5.4-fold) and of dATP in B-lymphocytes (4-fold) as well as with the inhibition of DNA synthesis, predominantly in T-lymphocytes. In both T- and B-lymphocytes, the dCTP pool was decreased. In the spleen, T- and B-lymphocytes of mice carrying transplantable 22 hepatoma 22 by the moment of its maximal growth (5th day), the DNA synthesis was inhibited as revealed by the reduction of (a) thymidine kinase activity, (b) rate of the labeled thymidine incorporation into DNA, and (c) intracellular dTTP and dCTP concentrations. In latter periods (from 8th day up to the moment of death), drastic stimulation of DNA synthesis in spleen T- and B-lymphocytes was observed irrespective of the impairments in the immune function and the decrease of the adenosine deaminase activity. In the course of growth of both transplantable and induced solid hepatomas in host spleen T- lymphocytes, the activity of the CTP-dependent thymidine kinase isoenzyme increased, coinciding in time with the activation of antigen-specific T-suppressors in the same organ.
在可移植性和邻氨基偶氮甲苯诱导的肝癌宿主(C3HA小鼠)的肝癌生长过程中,发现其脾脏免疫活性细胞(T淋巴细胞和B淋巴细胞)存在生化损伤。一旦肝癌出现(化学致癌过程),T淋巴细胞和B淋巴细胞中的腺苷脱氨酶和嘌呤核苷磷酸化酶活性分别降低了2至6倍和7至10倍,同时其免疫系统也受到损害。这些改变伴随着T淋巴细胞中dGTP浓度增加(5.4倍)和B淋巴细胞中dATP浓度增加(4倍),以及DNA合成受到抑制,主要是在T淋巴细胞中。在T淋巴细胞和B淋巴细胞中,dCTP池均减少。在携带可移植性肝癌22的小鼠脾脏中,在其生长至最大程度(第5天)时,T淋巴细胞和B淋巴细胞中的DNA合成受到抑制,这表现为:(a)胸苷激酶活性降低;(b)标记胸苷掺入DNA的速率降低;(c)细胞内dTTP和dCTP浓度降低。在后期(从第8天直至死亡),观察到脾脏T淋巴细胞和B淋巴细胞中的DNA合成受到剧烈刺激,而与免疫功能受损和腺苷脱氨酶活性降低无关。在宿主脾脏T淋巴细胞中可移植性和诱导性实体肝癌的生长过程中,依赖CTP的胸苷激酶同工酶活性增加,这与同一器官中抗原特异性T抑制细胞的激活在时间上相吻合。