In Mitochondria, It is Cytochrome c Oxidase that Absorbs Light and Affects Cellular Metabolism

In order for light therapy to work, light energy (which exists in little packets of energy called photons), must be absorbed by cells. It has been reported that there are many components of cells that are able to interact with light to affect cellular metabolism. A cellular enzyme in mammalian mitochondria, Cytochrome c oxidase, has been frequently studied as a photosensitive enzyme.

In a mitochondrion’s energy-producing process (which produces the energy for cells to live and function), cytochrome c oxidase is the final, crucial step. In the electron transport chain, it takes electrons from cytochrome c molecules, transfers them to an oxygen molecule, adds four protons to the mix and produces two molecules of water. In doing so, it moves protons across the mitochondria inner membrane that ultimately sparks the production of ATP, the cell’s fuel.

When exposed to light in the 670nm wavelength, cytochrome c oxidase is able to use that photonic energy and function very effectively.

From the Journal of Biological Chemistry: “Photobiomodulation Directly Benefits Primary Neurons Functionally Inactivated by Toxins”

Far-red and near-infrared (NIR) light promotes temporary relief from chronic pain, but the mechanism is poorly understood. Our previous studies using 670 nm light-emitting diode (LED) arrays suggest that cytochrome c oxidase, a photoacceptor in the NIR range, plays an important role in therapeutic photobiomodulation. If this is true, then an irreversible inhibitor of cytochrome c oxidase, potassium cyanide (KCN), should compete with LED and reduce its beneficial effects.

This hypothesis was tested on primary cultured neurons. LED treatment partially restored enzyme activity blocked by 10-100 µM KCN. It significantly reduced neuronal cell death induced by 300 µM KCN from 83.6% to 43.5%. However, at 1-100 mM KCN, the protective effects of LED decreased, and neuronal deaths increased. LED significantly restored neuronal ATP content only at 10 µM KCN, but not at higher concentrations of KCN tested. Pretreatment with LED enhanced efficacy of LED during exposure to 10 or 100 µM KCN, but did not restore enzyme activity to control levels. In contrast, LED was able to completely reverse the detrimental effect of tetrodotoxin, which only indirectly down-regulated enzyme levels. Among the wavelengths tested (670 nm, 728 nm, 770 nm, 830 nm, and 880 nm), the most effective ones (830 nm; 670 nm) paralleled the NIR absorption spectrum of oxidized cytochrome c oxidase, whereas the least effective wavelength, 728 nm, did not .

The results are consistent with our hypothesis that the mechanism of photobiomodulation involves the up-regulation of cytochrome c oxidase, leading to increased energy metabolism in neurons functionally inactivated by toxins.

The Journal of Biological Chemistry. Volume 280, Number 6, Issue of Februrary 11, pp 2761-4771, 2005. “Photobiomodulation Directly Benefits Primary Neurons Functionally Inactivated by Toxins. Role of Cytochrome C Oxidase.” © 2005 by the American Society for Biochemistry and Molecular Biology, Inc.

This website is intended for healthcare professionals and clinical researchers only. All of the treatments using LED phototherapy devices that are discussed on this website are in various stages of investigation and have not been approved by the FDA except where specifically stated.

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