Objective: The objective of this work is to put forward a mechanism by which low-level light [red-to near infrared (NIR) laser or light emitting diodes (LED)] is instrumental in the process of accelerating the healing of wounds.
Background data: Interaction modalities of low-level light with oxidatively stressed cells and tissues are the focus of intense research efforts. Several models of the light/cell-interaction mechanism have been proposed. In the most popular model, cytochrome c oxidase is believed to play the role of the principal acceptor for red-to NIR photons.
Methods: Using as an illustrative example the successful LED treatment of an edematous limb ulcer, the results of recent in vitro tests and complementary laboratory experiments are presented and discussed.
Results: The most plausible mechanism of biostimulatory effect of red-to NIR light consists of its impact on the nanoscopic interfacial water layers in mitochondria and the extracellular matrix (ECM) where mitochondrial reactive oxygen species (ROS) induce an increase in the viscosity of the water layers bound to the predominantly hydrophilic surfaces in the intramitochondrial space as well as the ECM, where the process progressively propagates with age. The biostimulatory effect of red-to NIR light consists of counteracting the ROS-induced elevation of interfacial water viscosities, thereby instantly restoring the normal mitochondrial function, including the synthesis of adenosine triphosphate (ATP) by the rotary motor (ATP synthase).
Conclusions: An understanding of the mechanism of interaction of red-to NIR light with mitochondria, cells, and tissues safeguards progress in the field of low-level light therapy (LLLT) and puts us in the position to design better therapies.
Keywords: ATP; LED; ROS; interfacial water viscosity; laser; mitochondria; wound.