Jones C A, Huberman E, Cunningham M L, Peak M J
Radiat Res. 1987 May;110(2):244-54.
Action spectra were determined for cell killing and mutation by monochromatic ultraviolet and visible radiations (254-434 nm) in cultured human epithelial P3 cells. Cell killing was more efficient following radiation at the shorter wavelengths (254-434 nm) than at longer wavelengths (365-434 nm). At 254 nm, for example, a fluence of 11 Jm-2 gave 37% cell survival, while at 365 nm, 17 X 10(5) Jm-2 gave equivalent survival. At 434 nm little killing was observed with fluences up to 3 X 10(6) Jm-2. Mutant induction, determined at the hypoxanthine-guanine phosphoribosyltransferase locus, was caused by radiation at 254, 313, and 365 nm. There was no mutant induction at 334 nm although this wavelength was highly cytotoxic. Mutagenesis was not induced by 434 nm radiation, either. There was a weak response at 405 nm; the mutant frequencies were only slightly increased above background levels. For the mutagenic wavelengths, log-log plots of the mutation frequency against fluence showed linear regressions with positive slopes of 2.5, consistent with data from a previous study using Escherichia coli. The data points of the action spectra for lethality and mutagenesis were similar to the spectrum for DNA damage at wavelengths shorter than 313 nm, whereas at longer wavelengths the lethality spectrum had a shoulder, and the mutagenesis spectrum had a secondary peak at 365 nm. No correlation was observed for the P3 cells between the spectra for cell killing and mutagenesis caused by wavelengths longer than 313 nm and the induction of DNA breakage or the formation of DNA-to-protein covalent bonds in these cells.
通过单色紫外线和可见光辐射(254 - 434nm)对培养的人上皮P3细胞进行细胞杀伤和突变的作用光谱已被测定。在较短波长(254 - 434nm)下辐射后细胞杀伤比在较长波长(365 - 434nm)下更有效。例如,在254nm时,11Jm-2的通量产生37%的细胞存活率,而在365nm时,17×10(5)Jm-2产生相同的存活率。在434nm时,通量高达3×10(6)Jm-2时几乎未观察到细胞杀伤。在次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶位点测定的突变诱导是由254、313和365nm的辐射引起的。在334nm时没有突变诱导,尽管该波长具有高度细胞毒性。434nm辐射也未诱导诱变。在405nm时有微弱反应;突变频率仅略高于背景水平增加。对于诱变波长,突变频率与通量的双对数图显示线性回归,正斜率为2.5,与先前使用大肠杆菌的研究数据一致。致死率和诱变作用光谱的数据点在波长小于313nm时与DNA损伤光谱相似,而在较长波长时,致死率光谱有一个肩部,诱变光谱在365nm时有一个次级峰。对于波长大于313nm的细胞杀伤光谱和诱变光谱与这些细胞中DNA断裂的诱导或DNA - 蛋白质共价键的形成之间,未观察到P3细胞的相关性。