Photon Factory, Institute of Material Science, High Energy Accelerator Research Organization, 1-1 Oho, Tsukuba, Ibaraki 305-0801, Japan.
Department of Oncology, Kagoshima University Graduate School of Medical and Dental Sciences, 8-35-1, Sakuragaoka, Kagoshima 890-8544, Japan.
J Radiat Res. 2020 Mar 23;61(2):237-242. doi: 10.1093/jrr/rrz098.
The aim of this study was to determine whether membrane lipid peroxidation in mammalian cells is enhanced by X-ray irradiation at the K-shell resonance absorption peak of phosphorus. A549 and wild-type p53-transfected H1299 (H1299/wtp53) cell lines derived from human lung carcinoma were irradiated with monoenergetic X-rays at 2.153 keV, the phosphorus K-shell resonance absorption peak, or those at 2.147 or 2.160 keV, which are off peaks. Immunofluorescence staining for 4-hydroxy-2-nonenal (HNE), a lipid peroxidation product, was used as marker for protein modification. In both cell lines, the HNE production was significantly enhanced after irradiation at 2.153 keV compared to sham-irradiation. The enhancement (E) was calculated as the ratio of the fluorescence intensity of irradiated cells to that of sham-irradiated cells. In both the cell lines, E2.153 was significantly larger than E2.147 and no significant difference between E2.147 and E2.160 was observed. The extra enhancement at 2.153 keV was possibly caused by energy transition within the phosphorus K-shell resonance absorption. Our results indicate that membrane lipid peroxidation in cells is enhanced by the Auger effect after irradiation at the K-shell resonance absorption peak of phosphorus rather than by the photoelectric effect of the constituent atoms in the membrane lipid at 2.147 keV.
本研究旨在确定哺乳动物细胞的膜脂质过氧化是否会因 X 射线在磷的 K 壳共振吸收峰处的辐照而增强。从人肺癌衍生而来的 A549 和野生型 p53 转染的 H1299（H1299/wtp53）细胞系用单能 X 射线在 2.153keV（磷 K 壳共振吸收峰）、2.147keV 或 2.160keV（非共振峰）处进行辐照。4-羟基-2-壬烯醛（HNE）的免疫荧光染色，作为蛋白质修饰的标志物。在这两种细胞系中，与假照射相比，在 2.153keV 处辐照后 HNE 的产生明显增强。增强（E）的计算方法是将照射细胞的荧光强度与假照射细胞的荧光强度进行比较。在这两种细胞系中，E2.153 明显大于 E2.147，E2.147 和 E2.160 之间没有观察到显著差异。2.153keV 处的额外增强可能是由于磷 K 壳共振吸收内的能量跃迁引起的。我们的结果表明，细胞中的膜脂质过氧化是由磷的 K 壳共振吸收处的俄歇效应而不是膜脂质中组成原子的光电效应在辐照后增强的。
