Sommer Andrei P, Schemmer Peter, Pavláth Attila E, Försterling Horst-Dieter, Mester Ádám R, Trelles Mario A
Faculty of Science, ISRA University, Amman, Jordan.
General, Visceral and Transplant Surgery, Medical University of Graz, Graz, Austria.
Ann Transl Med. 2020 Apr;8(7):440. doi: 10.21037/atm.2020.03.159.
It is shown that despite exponential increase in the number of clinically exciting results in low level light therapy (LLLT), scientific progress in the field is retarded by a wrong fundamental model employed to explain the photon-cell interaction as well as by an inadequate terminology. This is reflected by a methodological stagnation in LLLT, persisting since 1985. The choice of the topics is, by necessity, somewhat arbitrary. Obviously, we are writing more about the fields we know more about. In some cases, there are obvious objective reasons for the choice. Progress in LLLT is currently realized by a trial and error process, as opposed to a systematic approach based on a valid photon-cell interaction model.
The strategy to overcome the current problem consists in a comprehensive analysis of the theoretical foundation of LLLT, and if necessary, by introducing new interaction models and checking their validity on the basis of the two pillars of scientific advance (I) agreement with experiment and (II) predictive capability. The list of references used in this work, does contain a representative part of what has been done in the photon-cell interaction theory in recent years, considered as ascertained by the scientific community.
Despite the immense literature on the involvement of cytochrome c oxidase (COX) in LLLT, the assumption that COX is the main mitochondrial photoacceptor for R-NIR photons no longer can be counted as part of the theoretical framework proper, at least not after we have addressed the misleading points in the literature. Here, we report the discovery of a coupled system in mitochondria whose working principle corresponds to that of field-effect transistor (FET). The functional interplay of cytochrome c (emitter) and COX (drain) with a nanoscopic interfacial water layer (gate) between the two enzymes forms a biological FET in which the gate is controlled by R-NIR photons. By reducing the viscosity of the nanoscopic interfacial water layers within and around the mitochondrial rotary motor in oxidatively stressed cells R-NIR light promotes the synthesis of extra adenosine triphosphate (ATP).
Based on the results of our own work and a review of the published literature, we present the effect of R-NIR photons on nanoscopic interfacial water layers in mitochondria and cells as a novel understanding of the biomedical effects R-NIR light. The novel paradigm is in radical contrast to the theory that COX is the main absorber for R-NIR photons and responsible for the increase in ATP synthesis, a dogma propagated for more than 20 years.
研究表明，尽管低强度光疗法（LLLT）在临床上令人兴奋的结果数量呈指数增长，但该领域的科学进展却因用于解释光子与细胞相互作用的错误基本模型以及术语使用不当而受到阻碍。这体现在自1985年以来LLLT在方法学上的停滞不前。主题的选择必然有些随意。显然，我们更多地是在撰写我们更了解的领域。在某些情况下，选择有明显的客观原因。目前LLLT的进展是通过试错过程实现的，而不是基于有效的光子与细胞相互作用模型的系统方法。
克服当前问题的策略包括对LLLT的理论基础进行全面分析，如有必要，引入新的相互作用模型，并根据科学进步的两大支柱（I）与实验的一致性和（II）预测能力来检验其有效性。本工作中使用的参考文献列表确实包含了近年来光子与细胞相互作用理论方面已完成工作的代表性部分，科学界认为这些工作已得到确认。
尽管有大量关于细胞色素c氧化酶（COX）参与LLLT的文献，但COX是R - NIR光子的主要线粒体光受体这一假设，至少在我们解决了文献中的误导性观点之后，已不能再被视为适当理论框架的一部分。在此，我们报告在线粒体中发现了一个耦合系统，其工作原理与场效应晶体管（FET）的原理相对应。细胞色素c（发射极）和COX（漏极）与这两种酶之间的纳米级界面水层（栅极）的功能相互作用形成了一种生物FET，其中栅极由R - NIR光子控制。通过降低氧化应激细胞中线粒体旋转马达内部及周围纳米级界面水层的粘度，R - NIR光促进了额外三磷酸腺苷（ATP）的合成。
基于我们自己的工作结果以及对已发表文献的综述，我们提出R - NIR光子对线粒体和细胞中纳米级界面水层的影响，作为对R - NIR光生物医学效应的一种新认识。这种新范式与COX是R - NIR光子的主要吸收体并负责ATP合成增加这一理论形成了鲜明对比，该理论已经流传了20多年。
