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阐明慢性炎症时吞噬细胞释出的某些内源性因子在辐射致癌中的作用。方法以C3H10T1/2和原代SHE为靶细胞,用238Pu为体外α照射源,用转化灶形成法观察PMA及其刺激人外周血产生的过量自由基、调理酵母多糖刺激U-937细胞释放的TNF-α等炎性因子对α粒子照射细胞转化频率(TF)的增加效应。结果PMA和它刺激的人血使0.5Gyα粒子照射的C3H10T1/2细胞的TF分别增高2.1和2.8倍。U-937释放的TNF-α炎症因子TF增高12倍;用抗TNF-α抗体中和后,证明U-937上清中仍有其他促癌因子存在。0.5Gyα粒子照射的SHE细胞在体外长期传代生长对hrTNF-α具有依赖性,由此得到的40代的细胞具有致瘤性。结论慢性炎症条件下,中性粒细胞和巨噬细胞释出的过量自由基和TNF-α等因子在低剂量辐射致癌中起重要作用。
To elucidate the role of certain endogenous factors released by phagocytes during radiation-induced carcinogenesis in chronic inflammation. Methods C3H10T1 / 2 and primary SHE were used as target cells, and 238Pu was used as in vitro α irradiation source. PMA and excess free radicals stimulated by human peripheral blood were observed by the method of foci formation. The effects of zymosan on the release of U-937 cells TNF-α and other inflammatory factors on the alpha particle irradiation frequency (TF) increased effect. Results PMA and its stimulated human blood increased TF of C3H10T1 / 2 cells irradiated by 0.5Gyα particles by 2.1 and 2.8 times, respectively. U-937 release of TNF-α inflammatory factor TF increased 12-fold; with anti-TNF-α antibody neutralization, U-937 showed that there are still other supernatants in the presence of other cancer-promoting agents. Long-term passage growth of SHE cells irradiated with 0.5Gyα particles was dependent on hrTNF-α, and the 40-generation cells thus obtained had tumorigenicity. Conclusions Chronic inflammatory conditions, excessive release of free radicals and TNF-α and other factors by neutrophils and macrophages play an important role in carcinogenesis induced by low doses of radiation.