Lewis Jill B, Wataha John C, Messer Regina L W, Caughman Gretchen B, Yamamoto Tetsuya, Hsu Stephen D
School of Dentistry, Department of Oral Biology & Maxillofacial Pathology, Medical College of Georgia, Augusta, Georgia 30912, USA.
J Biomed Mater Res B Appl Biomater. 2005 Feb 15;72(2):223-9. doi: 10.1002/jbm.b.30126.
Blue light (lambda = 380-500 nm) historically has been used to initiate polymerization of biomaterials and recently has been proposed as a therapeutic agent. New evidence suggests that cell-type-specific responses result from redox changes induced by exposure to blue light. Cultured cells were exposed to defined doses of blue light, equivalent to exposure times of 10 s and 2 min, to achieve energies of 5 J/cm2 and 60 J/cm2, respectively, after which (a) viable cell number, (b) cellular protein profiles, (c) mitochondrial succinate dehydrogenase (SDH) activity, (d) total reactive oxygen species (ROS), and (e) induction of apoptosis were compared to that of nonexposed control cultures. Results showed that blue-light exposure arrested monocyte cell growth and increased levels of peroxiredoxins. SDH activity of normal epidermal keratinocytes (NHEK) was slightly enhanced by blue light, whereas identical treatment of OSC2 oral tumor cells resulted in significant suppression of SDH activity. Blue-light exposure generally induced higher levels of total ROS in OSC2 cells than in NHEK. Finally, only OSC2 cells exhibited signs of apoptosis via Annexin V staining following exposure to blue light. These data support the central hypothesis that blue light induces an oxidative stress response in cultured cells resulting in cell-type-specific survival outcomes. The identification of oxidative stress as a mediator of the effects of blue light is a critical first step in defining its biological risks and therapeutic opportunities.
蓝光（波长λ = 380 - 500纳米）在历史上一直被用于引发生物材料的聚合反应，最近也被提议作为一种治疗剂。新的证据表明，细胞类型特异性反应是由暴露于蓝光引起的氧化还原变化所导致的。将培养的细胞暴露于特定剂量的蓝光下，相当于10秒和2分钟的暴露时间，分别达到5 J/cm²和60 J/cm²的能量，之后将（a）活细胞数量、（b）细胞蛋白质谱、（c）线粒体琥珀酸脱氢酶（SDH）活性、（d）总活性氧（ROS）以及（e）凋亡诱导情况与未暴露的对照培养物进行比较。结果显示，蓝光照射会阻止单核细胞的生长并增加过氧化物酶的水平。蓝光使正常表皮角质形成细胞（NHEK）的SDH活性略有增强，而对OSC2口腔肿瘤细胞进行相同处理则导致SDH活性显著抑制。蓝光照射通常在OSC2细胞中诱导产生的总ROS水平高于NHEK细胞。最后，只有OSC2细胞在暴露于蓝光后通过膜联蛋白V染色显示出凋亡迹象。这些数据支持了核心假设，即蓝光在培养细胞中诱导氧化应激反应，从而导致细胞类型特异性的存活结果。将氧化应激确定为蓝光效应的介导因素是定义其生物风险和治疗机会的关键第一步。
