Blue light exposure in vitro causes toxicity to trigeminal neurons and glia through increased superoxide and hydrogen peroxide generation
Blue light exposure in vitro causes toxicity to trigeminal neurons and glia through increased superoxide and hydrogen peroxide generation
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DOI：
10.1016/j.freeradbiomed.2018.11.029
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发表时间：
2019-02-01
影响因子：
7.4
通讯作者：
Parsadaniantz, S. Melik
中科院分区：
文献类型：
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作者：
Marek, V.;Potey, A.;Parsadaniantz, S. Melik
今天，在各种眼科疾病的背景下，来自自然和特别是人工(荧光管、LED面板、视觉显示器)来源的蓝光的毒性被积极地讨论。它们中的许多都有一个重要的神经系统成分，并与眼睛疼痛有关。这种神经病理信号是由三叉神经节的伤害性神经元提供的。然而，到目前为止，蓝光对三叉神经细胞的光毒性还没有被研究过。为探讨不同波段(410~630 nm)可见光对原代培养小鼠三叉神经细胞和神经胶质细胞的细胞毒性作用，以410、440和480 nm为中心的平均1.1 mW/cm的窄带蓝光照射3h可引起细胞死亡、细胞形态改变和氧化应激及炎症反应。在其他测试的可见波段中，没有观察到这些影响。我们观察到神经元和神经胶质细胞以不同的方式处理光信号，包括产生超氧化物和过氧化氢，炎性生物标记物的表达和光毒性线粒体损伤。我们分析了光信号接收的途径，提出在三叉神经细胞中，除了众所周知的线粒体介导的光吸收外，光还可以通过非视觉Opsins、黑素蛋白(Opn4)和神经蛋白(OPN5)接受。我们还研究了观察到的光毒性的机制，进一步表明内质网在蓝光毒性信息的神经元传递中发挥了重要作用。综上所述，我们的结果提供了一些关于在咨询这些眼部症状的患者中经常观察到的纠缠疼痛和光敏的电路的一些洞察。
Today the noxiousness of blue light from natural and particularly artificial (fluorescent tubes, LED panels, visual displays) sources is actively discussed in the context of various ocular diseases. Many of them have an important neurologic component and are associated with ocular pain. This neuropathic signal is provided by nociceptive neurons from trigeminal ganglia. However, the phototoxicity of blue light on trigeminal neurons has not been explored so far. The aim of the present in vitro study was to investigate the cytotoxic impact of various wavebands of visible light (410-630 nm) on primary cell culture of mouse trigeminal neural and glial cells.Three-hour exposure to narrow wavebands of blue light centered at 410, 440 and 480 nm of average 1.1 mW/cm(2) irradiance provoked cell death, altered cell morphology and induced oxidative stress and inflammation. These effects were not observed for other tested visible wavebands. We observed that neurons and glial cells processed the light signal in different manner, in terms of resulting superoxide and hydrogen peroxide generation, inflammatory biomarkers expression and phototoxic mitochondrial damage. We analyzed the pathways of photic signal reception, and we proposed that, in trigeminal cells, in addition to widely known mitochondria-mediated light absorption, light could be received by means of non-visual opsins, melanopsin (opn4) and neuropsin (opn5). We also investigated the mechanisms underlying the observed phototoxicity, further suggesting an important role of the endoplasmic reticulum in neuronal transmission of blue-light-toxic message. Taken together, our results give some insight into circuit of tangled pain and photosensitivity frequently observed in patients consulting for these ocular symptoms.