RESPIRATORY CARCINOGENESIS BY CHEMICAL AND PHYSICAL FACTORS

慢性肺肉芽肿病/纤维化在肺结核中的作用 在新的实验模型中研究了肺癌的诱导， 也就是说，二氧化硅的致癌作用 结晶二氧化硅形式（石英， 氢氟酸蚀刻石英、方石英和鳞石英） 将细颗粒注入近交系大鼠的气管内， 仓鼠和老鼠。 对石英和氢氟酸的长期研究- 酸蚀石英显示， 肺癌（主要是腺癌）， 女性 一系列的牺牲研究表明， 大鼠的反应之前是一个强烈的增生， 邻近区域的细支气管和肺泡（11型）上皮细胞 矽肺肉芽肿性病变。 上皮增生开始 在单次给予二氧化硅的几天内， 增殖性增生和腺瘤样病变， 转化为癌细胞 相比之下， 在仓鼠体内和在小鼠体内短暂存在。 到目前为止， 观察到，在肺中没有发现致癌反应， 仓鼠和小鼠，甚至在腺瘤倾向株A中。 标记 在结构和细胞形态上存在种间差异 肉芽肿反应的组成。 的相关性 上皮细胞增生伴邻近炎性细胞， 他们的调解人进行了调查有关主机的差异， 上皮细胞的细胞发病机制， 炎症/纤维化反应。 二甲亚砜（DMSO），腹腔注射，显着 内毒素增强呼吸道癌的发生 苯并（a）芘/氧化铁（BP）。 增强功能是 当同时给予DMSO时，而不是在给药后5天， 每支BP 放射自显影分析显示， 同时DMSO对单次BP剂量在 整个呼吸道。

The role of chronic pulmonary granulomatosis/fibrosis in the induction of lung cancer was studied in a new experimental model, i.e., carcinogenesis by silica. Crystalline silica forms (quartz, hydrofluoric-acid-etched quartz, cristobalite and tridymite) in fine particles were instilled intratracheally in inbred rats, hamsters and mice. Long-term studies with quartz and hydrofluoric- acid-etched quartz showed that rats developed high incidences of pulmonary carcinomas (mostly adenocarcinomas) with prevalence in females. Serial sacrifice studies showed that this carcinogenic response of the rat is preceded by an intense hyperplasia of the bronchiolar and alveolar (type 11) epithelia in areas adjacent to silicotic granulomatous lesions. The epithelial hyperplasia begins within days of single administrations of silica and progresses into proliferative hyperplasias and adenomatoid lesions, and ultimately into carcinomas. In contrast, the epithelial reaction was minimal in hamsters and transient in mice. Within the times so far observed, no carcinogenic response was found in the lungs of hamsters and mice, even in the adenoma-prone strain A. Marked species differences were identified in the structure and cellular composition of the granulomatous reaction. The correlation of epithelial proliferation with the adjacent inflammatory cells and their mediators is investigated in relation to host differences in the cellular pathogenesis of the epithelial and inflammatory/fibrogenic responses. Dimethylsulfoxide (DMSO), given intraperitoneally, markedly enhanced respiratory carcinogenesis by intratracheal benzo(a)pyrene/ferric oxide (BP) in hamsters. The enhancement was higher when DMSO was given concurrently rather than five days after each BP dose. Autoradiographic analysis showed no influence of concurrent DMSO on localization and binding of a single BP dose in the whole respiratory tract.