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实验性紫外线光致癌作用:波长相互作用及时间-剂量关系

Experimental ultraviolet photocarcinogenesis: wavelength interactions and time-dose relationships.

作者信息

Forbes P D, Davies R E, Urbach F

出版信息

Natl Cancer Inst Monogr. 1978 Dec(50):31-8.

PMID:753978
Abstract

Tumors were induced in the skin of SKH hairless mice by exposure to fluorescent FS sun lamps or to a long-arc xenon solar simulator. Tumores developed about equally well with varying amounts of UV-A radiation (lambda greater than 320 nm) given simultaneously. In contrast, incremental changes in the UV-B region (lambda less than 320 nm) led to substantial increases in carcinogenic effectiveness. A tumor-"initiating" dose of UV-B (4-10 wk of daily FS lamp exposures) was rendered less effective by subsequent exposures of the mice to UV-A (6 hr/day, F-40 T12BL lamps). The mechanism for this effect is not known. Most tumors induced by a short course (10 wk) of FS lamp exposure grew slowly or regressed, whereas mice exposed for a longer period (30 wk) developed more tumors, and many of those that appeared early grew aggressively. Effects of daily dose fractionation were less clear, and the subject requires further study. These and other variables are being tested in a program designed to yield useful information on the effects of changing spectrum, dose, and dose delivery rates on sunlight-induced cancer.

摘要

通过暴露于荧光FS太阳灯或长弧氙气太阳模拟器,在SKH无毛小鼠的皮肤上诱发肿瘤。同时给予不同剂量的UV - A辐射(波长大于320nm)时,肿瘤生长情况大致相同。相比之下,UV - B区域(波长小于320nm)的增量变化会导致致癌效力大幅增加。通过随后让小鼠暴露于UV - A(每天6小时,F - 40 T12BL灯),UV - B的肿瘤“启动”剂量(每天暴露于FS灯4 - 10周)效力降低。这种效应的机制尚不清楚。短疗程(10周)FS灯暴露诱导的大多数肿瘤生长缓慢或消退,而暴露时间较长(30周)的小鼠产生了更多肿瘤,并且许多早期出现的肿瘤生长迅速。每日剂量分割的影响不太明确,该主题需要进一步研究。这些及其他变量正在一个旨在提供关于光谱变化、剂量和剂量传递速率对阳光诱发癌症影响的有用信息的项目中进行测试。

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UVB-induced DNA breaks interfere with transcriptional induction of c-fos.紫外线B诱导的DNA断裂会干扰c-fos的转录诱导。
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