Peek At Science: 2023 January 31

Peak At Science 20230117
Quantum Biology

Peek At Science: 2023 January 31

Blue Light Induces Mitochondrial DNA Damage and Free Radical Production in Epithelial Cells

Exposure of biological chromophores to ultraviolet radiation can lead to photochemical damage. However, the role of visible light, particularly in the blue region of the spectrum, has been largely ignored. To test the hypothesis that blue light is toxic to non-pigmented epithelial cells, confluent cultures of human primary retinal epithelial cells were exposed to visible light (390-550 nm at 2.8 milliwatts/cm2) for up to 6 h. A small loss of mitochondrial respiratory activity was observed at 6 h compared with dark-maintained cells, and this loss became greater with increasing time. To investigate the mechanism of cell loss, the damage to mitochondrial and nuclear genes was assessed using the quantitative PCR. Light exposure significantly damaged mitochondrial DNA at 3 h (0.7 lesion/10 kb DNA) compared with dark-maintained controls. However, by 6 h of light exposure, the number of lesions was decreased in the surviving cells, indicating DNA repair. Isolated mitochondria exposed to light generated singlet oxygen, superoxide anion, and the hydroxyl radical. Antioxidants confirmed the superoxide anion to be the primary species responsible for the mitochondrial DNA lesions. The effect of lipofuscin, a photoinducible intracellular generator of reactive oxygen intermediates, was investigated for comparison. Exposure of lipofuscin-containing cells to visible light caused an increase in both mitochondrial and nuclear DNA lesions compared with non-pigmented cells. We conclude that visible light can cause cell dysfunction through the action of reactive oxygen species on DNA and that this may contribute to cellular aging, age-related pathologies, and tumorigenesis.



生物の発色団を紫外線にさらすと、光化学的な損傷を引き起こす。しかし、可視光線、特にスペクトルの青色領域の役割は、これまでほとんど無視されてきた。青色光は非色素性上皮細胞に毒性があるという仮説を検証するために、ヒト初代網膜上皮細胞のコンフルエント培養を可視光(390-550 nm2.8 milliwatts/cm2)に最大6時間まで暴露した。細胞喪失のメカニズムを調べるために、ミトコンドリアおよび核内遺伝子の損傷を定量的 PCR 法を用いて評価した。光照射により、3 時間後にミトコンドリア DNA は暗所維持対照と比較して有意に損傷した(0.7 lesion/10 kb DNA)。しかし、光照射 6 時間後までには、生存細胞において損傷数は減少しており、DNA の修復が確認された。光照射された単離ミトコンドリアは、一重項酸素、スーパーオキシドアニオン、ヒドロキシルラジカルを生成した。抗酸化物質により、スーパーオキシドアニオンがミトコンドリア DNA 損傷の主要な原因物質であることが確認された。光誘導性の細胞内活性酸素中間体生成物質であるリポフスチンの影響も比較検討した。リポフスチンを含む細胞を可視光に曝露すると、色素のない細胞と比較して、ミトコンドリアおよび核のDNA損傷の両方が増加することがわかった。可視光は、DNAに活性酸素を作用させることで細胞機能障害を引き起こし、これが細胞の老化、加齢に伴う病態、腫瘍形成に寄与している可能性があると結論づけた。

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