Plitta-Michalak Beata, Kolobynina Ksenia G, Qin Qinghua, Jain Ishita, Chen I-Peng, Henning Stefan, Volkmer Beate, Greinert Rüdiger, Tham Anja, Boukamp Petra, Rapp Alexander
Cell Biology and Epigenetics, Department of Biology, Technical University of Darmstadt, Schnittspahnstr. 10, Darmstadt, 64287, Germany.
Department of Chemistry, Faculty of Agriculture and Forestry, University of Warmia and Mazury, Plac Łódzki 4, Olsztyn, 10-957, Poland.
Sci Rep. 2025 Jul 1;15(1):22312. doi: 10.1038/s41598-025-08763-z.
Ultraviolet A and B (UVA 320-400 nm and UVB 280-320 nm) induced cyclobutane-pyrimidine dimers (CPDs) are the most critical lesions caused by environmental sun exposure. Here we show that CPD removal is accelerated when, in addition to UV, cells are simultaneously exposed to water-filtered near-infrared (nIR, 750-1600 nm). The described effect is dose-dependent on the nIR-dose and is found in skin keratinocytes and fibroblasts. Accelerated removal of CPDs, which coincides with chromatin relaxation and faster CPD recognition, occurs after nIR exposure. While nIR alone does not affect cellular survival, co-exposure to UVB leads to reduced cellular survival and an increased number of mutations. Increasing single strand break levels (SSB) occur transiently after nIR exposure and independent of reactive oxygen species (ROS) formation. These data suggest that the rate-limiting step in the NER repair process - damage recognition - is facilitated by nIR-induced chromatin relaxation, causing the accumulation of unnatural high levels of SSBs and single stranded DNA, unfavourable for the cell fate resulting in reduced survival and increased mutation rates. Since nIR modulates the UV-dependent damage response, risk estimation of solar radiation-induced DNA damage should not only consider the UV components but also include the nIR fraction of the solar spectrum.
紫外线A和B（UVA 320 - 400纳米和UVB 280 - 320纳米）诱导产生的环丁烷嘧啶二聚体（CPD）是环境阳光照射引起的最关键损伤。我们在此表明，当细胞除了暴露于紫外线外，还同时暴露于水过滤近红外光（nIR，750 - 1600纳米）时，CPD的去除会加速。所述效应在nIR剂量上呈剂量依赖性，且在皮肤角质形成细胞和成纤维细胞中均有发现。nIR暴露后会加速CPD的去除，这与染色质松弛和更快的CPD识别同时发生。虽然单独的nIR不影响细胞存活，但与UVB共同暴露会导致细胞存活率降低和突变数量增加。nIR暴露后会短暂出现单链断裂水平（SSB）增加，且与活性氧（ROS）的形成无关。这些数据表明，核苷酸切除修复（NER）过程中的限速步骤——损伤识别——因nIR诱导的染色质松弛而得到促进，导致非自然高水平的SSB和单链DNA积累，这对细胞命运不利，从而导致存活率降低和突变率增加。由于nIR调节紫外线依赖性损伤反应，太阳辐射诱导的DNA损伤风险评估不仅应考虑紫外线成分，还应包括太阳光谱中的nIR部分。
