Han 2018 MiP2018

From Bioblast
Mitochondrial functional changes elicited by a single near-infrared (670nm) exposure. Han_Presentation

Link: MiP2018

Han T, Sauve Y, Lemieux H (2018)

Event: MiP2018


Photobiomodulation (PBM) has been gaining an increased amount of attention as a potential mitochondria-targeting treatment option. PBM involves application(s) of light at near-infrared (NIR) spectrum (600-1,000nm) to a biological tissue which reportedly induces increased mitochondrial electron transport system’s complex IV, cytochrome c oxidase (COX) by causing dissociation of nitric oxide (NO) from COX’s oxygen binding site [1]. It is believed that the increased COX function leads to increased ATP production and subsequent activation of protective mechanisms. Reported effects of PBM include accelerated wound healing, increased toxin resistance, and anti-oxidative effects [2]. However, the mitochondrial functional changes associated with NIR light exposure remain controversial. The present study provides a detailed account of functional changes in mitochondria with a single 670nm light exposure with varying fluence throughout 24 hour period. High-resolution respirometry (Oxygraph 2k; Oroboros Instruments) was used to measure mitochondrial function. HEK293T cell lines were used to study real-time changes in mitochondria with 200mW/cm2 and 6.37mW/cm2 power density lights. Jurkat cell lines exposed to 0.5-, 5-, and 15J fluence of 670nm light (power density 6.37mW/cm2) were monitored at 1-, 3-, 6-, and 24 hour after the exposure. Fluence was adjusted with varying exposure time. The multiple substrate-inhibitor protocol allowed measurement of ROUTINE, LEAK, ETS respiration capacities, and COX function. Paired t-tests and Wilcoxon signed ranked test were carried out. p<0.05 were significant.

Contrary to the reported effect of NIR light exposure [2], decreased COX function was observed in Jurkat cells exposed to 0.5J fluence light at 1-, 3-, 6-, and 24 hour post-exposure. However, we also observed changed chemical background (respiration following azide titration, used to calculate COX function). The chemical background was increased in 3-, 6-, and 24 hour post-exposure 0.5J fluence light and 6.37mW/cm2 light exposed real-time cells. On the other hand, decreased chemical background was observed in 1-, and 6- hour post-exposure 15J fluence light and 200mW/cm2 light exposed real-time cells. Based on this preliminary result, we propose a set of events that can explain the observed changes. (1) Decreased COX function may arise from increased NO availability. (2) Increased chemical background can be explained by COX’s increased azide resistance; whereas (3) decreased chemical background can be explained by decreased oxygen consumption from non-mitochondrial sources such as NADPH oxidase.

β€’ Bioblast editor: Plangger M, Kandolf G β€’ O2k-Network Lab: CA Edmonton Lemieux H

Labels: MiParea: Respiration 

Organism: Human  Tissue;cell: Kidney, HEK 

Enzyme: Complex IV;cytochrome c oxidase 

Coupling state: LEAK, ROUTINE, ET 

HRR: Oxygraph-2k 


Han T(1), Sauve Y(1,2), Lemieux H(3)

  1. Dept Ophthalmol Vis Sci
  2. Dept Physiol
  3. Fac Saint-Jean; Univ Alberta, Canada. - [email protected]


  1. Buravlev EA, Zhidkova TV, Osipov AN, Vladimirov YA (2014) Are the mitochondrial respiratory complexes blocked by NO the targets for the laser and LED therapy? Lasers Med Sci 30:173–80.
  2. Hennessy M, Hamblin MR (2017) Photobiomodulation and the brain: a new paradigm. J Opt 19:013003.
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