GE Research, One Research Circle, Niskayuna, NY 12309, USA.
GE Current, a Daintree Company, East Cleveland, OH 44112, USA.
J Photochem Photobiol B. 2020 Aug;209:111899. doi: 10.1016/j.jphotobiol.2020.111899. Epub 2020 May 22.
UV-A and visible light are thought to excite endogenous photosensitizers in microbes, thereby initiating complex chemical interactions that ultimately kill cells. Natural solar-based disinfection methods have been adapted into commercial lighting technologies with varying degrees of reported efficacy and associated safety hazards for human exposure. Here we utilize a narrow-spectrum UV-A LED prototype (currently in development for health care applications) to investigate the mechanism of bacterial photoinactivation using 365 nm light. Using a combination of reverse genetics and biochemical investigation, we report mechanistic evidence that 365nm light initiates a chain-reaction of superoxide-mediated damage via auto-excitation of vitamin-based electron carriers, specifically vitamin K2 menaquinones and the FAD flavoprotein in Complex II in the electron transport chain. We observe that photoinactivation is modifiable through supplementation of the environment to bypass cell damage. Lastly, we observe that bacteria forced into metabolic dormancy by desiccation become hypersensitized to the effects of UV-A light, thereby permitting photoinactivation at fluences that are significantly lower than the industry threshold for safe human exposure. In total, these results substantiate the mechanism and potential application of narrow- spectrum UV-A light for bacterial disinfection purposes.
紫外线-A 和可见光被认为会激发微生物中的内源性光敏剂,从而引发复杂的化学相互作用,最终杀死细胞。基于自然的太阳消毒方法已经被改编成商业照明技术,这些技术的报告疗效和人类暴露的相关安全危害程度各不相同。在这里,我们利用一种窄谱紫外线-A LED 原型(目前正在开发用于医疗保健应用),使用 365nm 光来研究细菌光灭活的机制。通过反向遗传学和生化研究的结合,我们报告了机制证据,表明 365nm 光通过维生素基电子载体的自激发引发了超氧化物介导的损伤的连锁反应,特别是维生素 K2 甲萘醌和电子传递链中复合物 II 中的 FAD 黄素蛋白。我们观察到,通过环境补充可以改变光灭活,从而避免细胞损伤。最后,我们观察到,通过干燥使细菌进入代谢休眠的细菌对紫外线-A 光的作用变得高度敏感,从而允许在比工业安全人类暴露阈值低得多的剂量下进行光灭活。总的来说,这些结果证实了窄谱紫外线-A 光用于细菌消毒的机制和潜在应用。