Differential effects of 808-nm light on electron transport chain enzymes in isolated mitochondria: Implications for photobiomodulation initiation

• Published in: Mitochondrion Vol. 68; pp. 15 - 24
• Main Authors: Pope, Nathaniel J., Denton, Michael L.
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.01.2023
• Subjects: Cytochrome c oxidase; Cytochrome c reductase; Electron Transport; Electron transport chain; Electron Transport Complex IV - metabolism; Enzyme kinetics; Low level light; Low-Level Light Therapy - methods; Mitochondria; Mitochondria - metabolism; Mitochondrial Membranes - metabolism; Photobiomodulation; Electron transport chain; Cytochrome c oxidase; Mitochondria; Cytochrome c reductase; Photobiomodulation; Enzyme kinetics; Low level light
• ISSN: 1567-7249; 1872-8278
• DOI: 10.1016/j.mito.2022.11.002

•Exposure to low-irradiance 808 nm light alters activity of mitochondrial enzymes.•Positively regulates complex IV, negatively regulates complex III.•Effect is dose-dependent and persists even after the light exposure ends.•Does not adhere to the Bunsen-Roscoe law of reciprocity (irradiance reciprocity).•Suggests this effect is not due to a direct photochemical mechanism. Photobiomodulation is a term for using low-power red to near-infrared light to stimulate a variety of positive biological effects. Though the scientific and clinical acceptance of PBM as a therapeutic intervention has increased dramatically in recent years, the molecular underpinnings of the effect remain poorly understood. The putative chromophore for PBM effects is cytochrome c oxidase. It is postulated that light absorption at cytochrome c oxidase initiates a signaling cascade involving ATP and generation of reactive oxygen species (ROS), which subsequently results in improved cellular robustness. However, this hypothesis is largely based on inference and indirect evidence, and the precise molecular mechanisms that govern how photon absorption leads to these downstream effects remain poorly understood. We conducted low-power PBM-type light exposures of isolated mitochondria to 808 nm NIR light, at a number of irradiances. NIR exposure was found to enhance the activity of complex IV, depress the activity of complex III, and had no effect on the activity of complex II. Further, examining the dose-response of complex IV we found NIR enhancement did not exhibit irradiance reciprocity, indicating the effect on complex IV may not have direct photochemical basis. In summary, this research presents a novel method to interrogate the earliest stages of PBM in the mitochondria, and a unique window into the corresponding molecular mechanism(s) of induction.