Spinardi A L, Kaneno R, Rodrigues M A, Salvadori D M, Rocha N S, Barbisan L F, Ribeiro L R, de Camargo J L
Department of Pathology, Faculty of Medicine, UNESP, Brazil.
Jpn J Cancer Res. 1999 Jan;90(1):101-7. doi: 10.1111/j.1349-7006.1999.tb00672.x.
Natural killer (NK) cell activity was evaluated after the initiation and promotion steps in a medium-term multi-organ bioassay for carcinogenesis. NK cell activity was assessed in vitro by Cr51 release assay at the 4th and 30th weeks of the experiment. Male Wistar rats were sequentially initiated with N-diethylnitrosamine (DEN i.p.), N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN drinking water), N-methyl-N-nitrosourea (MNU i.p.), dihydroxy-di-N-propylnitrosamine (DHPN drinking water) and N,N'-dimethylhydrazine (DMH s.c.) at subcarcinogenic doses for 4 weeks (DMBDD initiation). One group was evaluated at the 4th week and the other was maintained without any further treatment until the 30th week. Two initiated groups were exposed through the diet to 2-acetylaminofluorene (2-AAF) or phenobarbital (PB), from the 6th until the 30th week. Five additional groups were studied to evaluate the effects of each initiator on NK activity. All groups submitted to initiation only, initiation plus promotion, or promotion only, developed significantly more preneoplastic lesions than the untreated control group. The main target organs for tumor development in the initiated animals were the liver and the colon, irrespective of treatment with 2-AAF or PB. NK cell activity was not affected by exposure to genotoxic carcinogens after initiation, at the 4th week. Treatments only with PB or 2-AAF did not change NK cell activity. However, decreased NK cell activity was registered in the group only initiated with DMBDD and in the group given DMBDD+2-AAF. This late depression of NK cell activity at the 30th week could be related to the production of suppressing molecules by the tumor cells.
在一项中期多器官致癌生物测定的启动和促进步骤之后,对自然杀伤(NK)细胞活性进行了评估。在实验的第4周和第30周,通过铬51释放试验在体外评估NK细胞活性。雄性Wistar大鼠依次用亚致癌剂量的N-二乙基亚硝胺(腹腔注射)、N-丁基-N-(4-羟基丁基)亚硝胺(饮用水)、N-甲基-N-亚硝基脲(腹腔注射)、二羟基二-N-丙基亚硝胺(饮用水)和N,N'-二甲基肼(皮下注射)启动4周(DMBDD启动)。一组在第4周进行评估,另一组在不进行任何进一步处理的情况下维持到第30周。两个启动组从第6周直到第30周通过饮食接触2-乙酰氨基芴(2-AAF)或苯巴比妥(PB)。另外研究了五组以评估每种启动剂对NK活性的影响。所有仅接受启动、启动加促进或仅接受促进的组,与未处理的对照组相比,发生的癌前病变明显更多。启动动物中肿瘤发生的主要靶器官是肝脏和结肠,无论是否用2-AAF或PB处理。在第4周启动后,暴露于遗传毒性致癌物不会影响NK细胞活性。仅用PB或2-AAF处理不会改变NK细胞活性。然而,仅用DMBDD启动的组和给予DMBDD + 2-AAF的组中NK细胞活性降低。在第30周时NK细胞活性的这种后期降低可能与肿瘤细胞产生抑制分子有关。