Photobiomodulation with 808 nm laser light electively stimulates Complexes III and IV of the mitochondrial respiratory chain, while Complexes I and II are not affected. At the wavelength of 1064 nm, Complexes I, III, and IV are excited, while Complex II and some mitochondrial matrix enzymes seem to be not receptive to photons at that wavelength. Complex IV was also activated by 633 nm. The mechanism of action of wavelengths in the range 900–1000 nm on mitochondria is less understood or not described. Oxidative stress from reactive oxygen species (ROS) generated by mitochondrial activity is an inescapable consequence of aerobic metabolism. The antioxidant enzyme system for ROS scavenging can keep them under control. However, alterations in mitochondrial activity can cause an increment of ROS production. ROS and ATP can play a role in cell death, cell proliferation, and cell cycle arrest. In our work, bovine liver isolated mitochondria were irradiated for 60 sec, in continuous wave mode with 980 nm and powers from 0.1 to 1.4 W (0.1 W increment at every step) to generate energies from 6 to 84 J, fluences from 7.7 to 107.7 J/cm2, power densities from 0.13 to 1.79 W/cm2, and spot size 0.78 cm2. The control was equal to 0 W. The activity of the mitochondria’s complexes, Krebs cycle enzymes, ATP production, oxygen consumption, generation of ROS, and oxidative stress were detected. Lower powers (0.1–0.2 W) showed an inhibitory effect; those that were intermediate (0.3–0.7 W) did not display an effect, and the higher powers (0.8–1.1 W) induced an increment of ATP synthesis. Increasing the power (1.2–1.4 W) recovered the ATP production to the control level. The interaction occurred on Complexes III and IV, as well as ATP production and oxygen consumption. Results showed that 0.1 W uncoupled the respiratory chain and induced higher oxidative stress and drastic inhibition of ATP production. Conversely, 0.8 W kept mitochondria coupled and induced an increase of ATP production by increments of Complex III and IV activities. An augmentation of oxidative stress was also observed, probably as a consequence of the increased oxygen consumption and mitochondrial isolation experimental conditions. No effect was observed using 0.5 W, and no effect was observed on the enzymes of the Krebs cycle.

Background: Under physiological conditions, endothelial cells are the main regulator of arterial tone homeostasis and vascular growth, sensing and transducing signals between tissue and blood. Disease risk factors can lead to their unbalanced homeostasis, known as endothelial dysfunction. Red and near-infrared light can interact with animal cells and modulate their metabolism upon interaction with mitochondria’s cytochromes, which leads to increased oxygen consumption, ATP production and ROS, as well as to regulate NO release and intracellular Ca2+ concentration. This medical subject is known as photobiomodulation (PBM). We present a review of the literature on the in vitro and in vivo effects of PBM on endothelial dysfunction. Methods: A search strategy was developed consistent with the PRISMA statement. The PubMed, Scopus, Cochrane, and Scholar electronic databases were consulted to search for in vitro and in vivo studies. Results: Fifty out of >12,000 articles were selected. Conclusions: The PBM can modulate endothelial dysfunction, improving inflammation, angiogenesis, and vasodilatation. Among the studies, 808 nm and 18 J (0.2 W, 2.05 cm2) intracoronary irradiation can prevent restenosis as well as 645 nm and 20 J (0.25 W, 2 cm2) can stimulate angiogenesis. PBM can also support hypertension cure. However, more extensive randomised controlled trials are necessary.

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Diminished facial movement and marked facial asymmetry can lead to a consistent psychological burden. Bell′s palsy (BP) is one of the most common causes of facial nerve illness, which comes with unilateral acute facial paresis. Nowadays, no clear guidelines for treating BP are available. We carried out a case series study to test the efficacy of photobiomodulation (PBM) therapy in patients with BP non-responsive to standard treatment. The study was experimentally performed at the Department of Surgical and Diagnostic Sciences, University of Genoa (Genoa, Italy), in accordance with case report guidelines. Patients were referred to our department by colleagues for evaluation to be included in the case series because no consistent improvement was observed at least 3 months from the diagnosis of BP. All the patients interrupted their pharmacological therapy before the initiation of PBM therapy. PBM therapy (808 nm, 1 W irradiated in continuous-wave for 60 s on spot-size 1 cm2; 1 W/cm2; 60 J/cm2; and 60 J) was administered every 2 days until complete resolution. Evaluation of the House-Brackmann scale was performed before and after treatments. Fourteen patients were screened as eligible for the study. Patients were Caucasians (36% females and 64% males) with a mean age ± standard deviation of 56.07 ± 15.21 years. Eleven patients out of 14, who experienced BP a maximum of 6 months, completely recovered through PBM. The three patients that did not show improvement were those who had experienced BP for years. PBM could be a supportive therapy for the management of BP in patients non-responsive to standard treatment. However, randomized controlled trials are necessary to sustain our encouraging results, exclude bias, and better explain the boundary between the time from diagnosis and the recovery of BP through PBM therapy.

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