Near-infrared light at 810 nm increases mitochondrial membrane potential by 30% and ATP synthesis by 22%, mechanism demonstrated via cytochrome c oxidase.
This study by Hamblin et al. (2023), published in the Journal of Photochemistry and Photobiology, elucidates the fundamental mechanism by which near-infrared (NIR) light produces its biological effects: stimulation of cytochrome c oxidase (complex IV) of the mitochondrial respiratory chain.
The researchers used primary cell cultures and ex vivo muscle tissue models to precisely quantify the effects of irradiation at 810 nm on mitochondrial bioenergetic parameters, in particular membrane potential (ΔΨm) and ATP production.
The study provides robust mechanistic confirmation of the scientific efficacy of PBM, by showing that the observed effects are not non-specific but result from a precise photochemical interaction with an identified mitochondrial chromophore.
Primary cultures of human myocytes and murine cortical neurons. Mitochondria isolated from bovine liver tissue. Ex vivo muscle biopsies treated within 4 hours of harvest.
Source: 810 nm diode laser, power density 10–50 mW/cm². Tested doses: 0.5, 1, 2, 5, 10, 20 and 50 J/cm² to establish the dose-response curve (biphasic Arndt-Schulz effect).
Mitochondrial membrane potential (JC-1 fluorescence). ATP production (luciferase). Oxygen consumption (Seahorse XF analyzer). Cytochrome c oxidase activity (spectrophotometry).
Selective inhibition of complex IV (sodium azide, cyanide) to confirm the specificity of the effect on CCO. Thermal controls to exclude artifacts related to temperature elevation.
This mechanistic study is fundamental to understanding why photobiomodulation produces such varied effects, from muscle recovery to cognitive optimization. Everything rests on a single mechanism: stimulation of cytochrome c oxidase and increased ATP production in all exposed cells.
Confirmation of the biphasic dose-response curve is critical for our scientific practice. It justifies our approach of precise dosimetry: a dose that is too low is ineffective, a dose that is too high may become inhibitory. Our protocols are calibrated to systematically remain within the optimal therapeutic window identified (1–5 J/cm² depending on the target tissue).
The release of nitric oxide by CCO explains the vascular effects of PBM: improved microcirculation, reduced blood pressure, better tissue oxygenation. These effects particularly benefit patients with circulatory disorders or chronic fatigue of metabolic origin.
The discovery that the effect is abolished by specific CCO inhibitors (azide, cyanide) definitively confirms the specificity of the light-mitochondria interaction, ruling out any placebo or thermal effect in the scientific results obtained.