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<p>Ultraviolet A and B (UVA 320–400&#xa0;nm and UVB 280–320&#xa0;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&#xa0;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.</p>

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Exposure of cells to near-infrared irradiation relaxes chromatin compaction and facilitates recognition of cyclo-butane pyrimidine dimers

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月1日

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  • Beata Plitta-Michalak,
  • Ksenia G Kolobynina,
  • Qinghua Qin,
  • Ishita Jain,
  • I-Peng Chen,
  • Stefan Henning,
  • Beate Volkmer,
  • Rüdiger Greinert,
  • Anja Tham,
  • Petra Boukamp,
  • Alexander Rapp

摘要

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.