Mitochondrial solar sensitivity: evolutionary and biomedical implications

摘要

Depending on cellular demand or oxidative stress, mitochondria produce adenosine triphosphate (ATP) or reactive oxygen species (ROS), thereby controlling the entire scale of cellular energy supply or disease, respectively. While deficiency in ROS can compromise the immune system, excessive ROS levels contribute to a large number of pathological conditions, including retinal, neurodegenerative and cardiovascular disease as well as cancer. Aging is also a process accelerated by ROS. There is one noninvasive tool allowing us to precisely control both mitochondrial ATP and ROS: red-to-near infrared (R-NIR) light. The understanding why and how R-NIR light interacts with mitochondria was missing so far in the literature. Here we present a unified model for the interaction of R-NIR photons with three mitochondrial key players involved in ATP and ROS generation: ATP synthase, cytochrome c (CYTc) and cytochrome c oxidase (COX). The new model allows us to predictably control ATP and ROS generation in mitochondria by R-NIR light. Furthermore, comparison of the action spectrum of R-NIR light related to mitochondrial ATP and ROS generation with the spectral solar irradiance on Earth, puts us in the position to propose an evolutionary model describing the coordinated interplay of solar irradiation and water on the development of mitochondria on Earth. It accurately predicts which wavelengths of light provides maximum benefit for any desired clinical application and provides valuable hints regarding a time point for the evolutionary provenance of the mitochondrion.