Curriculum in Toxicology, University of North Carolina at Chapel Hill, Chapel Hill, NC.
The University of Texas MD Anderson Cancer Center, Science Park/Research Division, University of North Carolina at Chapel Hill, Chapel Hill, NC.
Photochem Photobiol. 2014 Jan;90(1):145-54. doi: 10.1111/php.12194. Epub 2013 Nov 28.
This study compared biological responses of normal human fibroblasts (NHF1) to three sources of ultraviolet radiation (UVR), emitting UVC wavelengths, UVB wavelengths, or a combination of UVA and UVB (solar simulator; emission spectrum, 94.3% UVA and 5.7% UVB). The endpoints measured were cytotoxicity, intra-S checkpoint activation, inhibition of DNA replication and mutagenicity. Results show that the magnitude of each response to the indicated radiation sources was best predicted by the density of DNA cyclobutane pyrimidine dimers (CPD). The density of 6-4 pyrimidine-pyrimidone photoproducts was highest in DNA from UVC-irradiated cells (14% of CPD) as compared to those exposed to UVB (11%) or UVA-UVB (7%). The solar simulator source, under the experimental conditions described here, did not induce the formation of 8-oxo-7,8-dihydroguanine in NHF1 above background levels. Taken together, these results suggest that CPD play a dominant role in DNA damage responses and highlight the importance of using endogenous biomarkers to compare and report biological effects induced by different sources of UVR.
本研究比较了正常人类成纤维细胞（NHF1）对三种紫外线辐射源（UVC 波长、UVB 波长或 UVA 和 UVB 的组合（太阳模拟器；发射光谱，94.3%UVA 和 5.7%UVB））的生物反应。测量的终点包括细胞毒性、S 期内检验点激活、DNA 复制抑制和致突变性。结果表明，每种辐射源的反应程度均与 DNA 环丁烷嘧啶二聚体（CPD）的密度密切相关。与接受 UVB（11%）或 UVA-UVB（7%）照射的细胞相比，UVC 照射的细胞中 6-4 嘧啶-嘧啶酮光产物的密度最高（占 CPD 的 14%）。在所描述的实验条件下，太阳模拟器源并未在 NHF1 中诱导 8-氧-7,8-二氢鸟嘌呤的形成，高于背景水平。综上所述，这些结果表明 CPD 在 DNA 损伤反应中起主导作用，并强调了使用内源性生物标志物来比较和报告不同来源 UVR 诱导的生物效应的重要性。
