van den Brenk H A, Kelly H, Holland K L
Br J Cancer. 1978 Jan;37(1):92-104. doi: 10.1038/bjc.1978.14.
Clonogenic growth (colony-forming efficiency, CFE) of i.v. injected allogeneic W256 tumour cells in the lungs was markedly enhanced by treatment of rats with alpha-naphthyl thiourea (ANTU) injected i.p. from 2 h before to 2 h after the tumour cells. ANTU specifically increases pulmonary vascular permeability in adult rats and causes acute pulmonary oedema and pleural effusion. Inhibition of drug toxicity to the lungs by tachyphylaxis, specific antimetabolites or iodides did not abolish the effect of ANTU on CFE. CFE was not increased when cells were seeded by i.v. injection the lungs affected by advanced pulmonary oedema at 6 to 24 h after treatment with drug. ANTU did not enhance growth of intratracheally injected cells. Although ANTU has no cytotoxic or immunosuppressive action, treatment of tumour-immunized rats with ANTU caused apparent "breakdown" of tumour immunity in 50% of rats, by causing growth of tumour colonies in the lungs. Possible mechanisms for the ANTU-induced decrease in innate resistance to growth of tumour in the lungs are discussed.
腹腔注射α-萘基硫脲(ANTU)处理大鼠,从静脉注射异基因W256肿瘤细胞前2小时至注射后2小时,肺部静脉注射的肿瘤细胞的克隆生长(集落形成效率,CFE)显著增强。ANTU可特异性增加成年大鼠肺血管通透性,并导致急性肺水肿和胸腔积液。速发性过敏反应、特异性抗代谢物或碘化物对肺部药物毒性的抑制作用并不能消除ANTU对CFE的影响。在用药物治疗6至24小时后,当通过静脉注射将细胞接种到受晚期肺水肿影响的肺部时,CFE并未增加。ANTU不会增强气管内注射细胞的生长。尽管ANTU没有细胞毒性或免疫抑制作用,但用ANTU处理肿瘤免疫大鼠会导致50%的大鼠出现明显的肿瘤免疫“破坏”,原因是肺部肿瘤集落生长。文中讨论了ANTU诱导肺部肿瘤生长先天抵抗力降低的可能机制。