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RESPIRATORY CARCINOGENESIS BY CHEMICAL AND PHYSICAL FACTORS

RESPIRATORY CARCINOGENESIS BY CHEMICAL AND PHYSICAL FACTORS
化学和物理因素导致的呼吸道致癌
批准号:
3963455
负责人:
U SAFFIOTTI
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
从不同节段的上皮细胞中诱导癌症 通过多因素机制在动物模型中的呼吸道, 通过化学、物理和化学方法的组合进行研究, 生物因素。 治疗开始时的年龄是一个重要因素 在二乙基亚硝胺诱导呼吸道肿瘤中, 段的具体方式。 在出生后接受治疗的仓鼠中, 鼻癌的发病率增加,潜伏期缩短, 仓鼠从8周龄开始;无显著的年龄相关影响 在诱导气管或肺肿瘤时发现。 并发 腹腔注射二甲亚砜可增加发病率, 严重程度,并减少呼吸道肿瘤诱导的潜伏期 苯并[a]芘(BP)混悬液经皮给药 与氧化亚铁。 一个复杂的多因素实验, 仓鼠的致癌作用已经完成,结果正在进行中。 分析;初步结果表明,单剂量的 N-甲基-N-亚硝基脲(MNU)在一系列BP/氧化铁前2周 给药显著增强喉和支气管癌的发生 相对于单独暴露于任一致癌物。 局部损伤 气管增强BP/氧化铁的致癌作用不仅在 气管也有支气管 既往暴露于BP/氧化铁 在所有暴露的呼吸道分泌物中增加BP的DNA结合 气管显示最高和最短暂的结合 程度. 研究二氧化硅诱导的肺上皮增生性病变, 它们与肉芽肿细胞反应和 炎症的细胞介质,与长期 不同形式的二氧化硅(石英,方石英, 鳞石英)。
英文摘要
The induction of cancers from the epithelia of the different segments of the respiratory tract in animal models by multifactorial mechanisms is studied by treatments with combinations of chemical, physical and biological factors. Age at beginning of treatment is an important factor in the induction of respiratory tumors by diethylnitrosamine in a segment-specific manner. In hamsters treated from birth, there is an increased incidence and decreased latency of nasal cancers, in comparison with hamsters started at 8 weeks of age; no significant age-related effect was found on the induction of tracheal or lung neoplasms. Concurrent intraperitoneal injection of dimethylsulfoxide increased the incidence and severity and decreased the latency of respiratory tumors induced by intratracheal administation of suspensions of benzo[a]pyrene (BP) combined with ferrix oxide. A complex multifactorial experiment of respiratory carcinogenesis in hamsters has been completed and the results are under analysis; preliminary results show that a single dose of N-methyl-N-nitrosourea (MNU) 2 weeks prior to a series of BP/ferric oxide administrations markedly enhances laryngeal and bronchial carcinogenesis relative to exposure to either carcinogen alone. Localized injury to the trachea enhances the carcinogenic effect of BP/ferric oxide not only in the trachea, but also in the bronchi. Previous exposure to BP/ferric oxide increases DNA binding of BP in all exposed slegments of the respiratory tract, with the trachea showing the highest and the most transient binding levels. Silica-induced pulmonary epithelial proliferative lesions are studied for their pathogenetic relationship to granulomatous cell reaction and to cellular mediators of inflammation, in conjunction with long-term carcinogenesis studies of different forms of silica (quarta, cristobalite, tridymite).
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