Mantovani A, Vecchi A, Luini W, Sironi M, Candiani G P, Spreafico F, Garattini S
Biomedicine. 1980 Dec;32(4):200-4.
C57Bl/6 J mice (6-8 weeks old) were given single i. p. doses (1, 2, 6 and 30 micrograms/kg) of 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD) and macrophage-mediated and natural killer (NK) cell-mediated cytotoxicity was evaluated at different times after treatment. Peritoneal macrophage cytolytic activity was measured as 3H-thymidine release from prelabelled mKSATU5 target cells in a 48 hours assay; macrophage-mediated cytostasis was assessed in terms of inhibitions of 3H-thymidine uptake by SL2 lymphoma cells. Spleen NK activity was measured using 51Cr-labelled YAC-1 lymphoma cells as targets. TCDD did not modify spontaneous macrophage-mediated and NK cell-mediated cytotoxicity per unit number of effector cells nor did it affect the macrophages' capacity to express increased cytolytic and cytostatic activity in the presence of endotoxin. Lower numbers of peritoneal macrophages and splenocytes were recovered from TCDD treated mice. Thus the total numbers of lytic units recovered from animals exposed to TCDD were lower than controls. Impairment of these cellular effector mechanisms, due to cell loss rather than inhibition of function, might play a role in the lowered resistance to bacterial infection of mice given TCDD and in the carcinogenic and cocarcinogenic activity of this chemical.
给6至8周龄的C57Bl/6 J小鼠腹腔注射单次剂量（1、2、6和30微克/千克）的2,3,7,8-四氯二苯并对二恶英（TCDD），并在处理后的不同时间评估巨噬细胞介导的和自然杀伤（NK）细胞介导的细胞毒性。在48小时的试验中，通过测量预标记的mKSATU5靶细胞中3H-胸腺嘧啶核苷的释放来测定腹腔巨噬细胞的溶细胞活性；根据SL2淋巴瘤细胞对3H-胸腺嘧啶核苷摄取的抑制作用来评估巨噬细胞介导的细胞生长抑制作用。使用51Cr标记的YAC-1淋巴瘤细胞作为靶标来测量脾脏NK活性。TCDD不会改变每单位效应细胞数量的自发巨噬细胞介导的和NK细胞介导的细胞毒性，也不会影响巨噬细胞在内毒素存在下表达增加的溶细胞和细胞生长抑制活性的能力。从TCDD处理的小鼠中回收的腹腔巨噬细胞和脾细胞数量较少。因此，从暴露于TCDD的动物中回收的裂解单位总数低于对照组。由于细胞损失而非功能抑制导致的这些细胞效应机制的损害，可能在给予TCDD的小鼠对细菌感染的抵抗力降低以及该化学物质的致癌和促癌活性中起作用。
