Inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury
Abstract The interaction of light with biological tissue has been successfully utilized for multiple therapeutic purposes. Previous studies have suggested that near infrared light (NIR) enhances the activity of mitochondria by increasing cytochrome c oxidase (COX) activity, which we confirmed for 81...
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oai:doaj.org-article:d38358554de345238b2771e0cebf73a72021-12-02T11:40:45ZInhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury10.1038/s41598-018-21869-x2045-2322https://doaj.org/article/d38358554de345238b2771e0cebf73a72018-02-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-21869-xhttps://doaj.org/toc/2045-2322Abstract The interaction of light with biological tissue has been successfully utilized for multiple therapeutic purposes. Previous studies have suggested that near infrared light (NIR) enhances the activity of mitochondria by increasing cytochrome c oxidase (COX) activity, which we confirmed for 810 nm NIR. In contrast, scanning the NIR spectrum between 700 nm and 1000 nm revealed two NIR wavelengths (750 nm and 950 nm) that reduced the activity of isolated COX. COX-inhibitory wavelengths reduced mitochondrial respiration, reduced the mitochondrial membrane potential (ΔΨm), attenuated mitochondrial superoxide production, and attenuated neuronal death following oxygen glucose deprivation, whereas NIR that activates COX provided no benefit. We evaluated COX-inhibitory NIR as a potential therapy for cerebral reperfusion injury using a rat model of global brain ischemia. Untreated animals demonstrated an 86% loss of neurons in the CA1 hippocampus post-reperfusion whereas inhibitory NIR groups were robustly protected, with neuronal loss ranging from 11% to 35%. Moreover, neurologic function, assessed by radial arm maze performance, was preserved at control levels in rats treated with a combination of both COX-inhibitory NIR wavelengths. Taken together, our data suggest that COX-inhibitory NIR may be a viable non-pharmacologic and noninvasive therapy for the treatment of cerebral reperfusion injury.Thomas H. SandersonJoseph M. WiderIcksoo LeeChristian A. ReynoldsJenney LiuBradley LeporeReneé TousignantMelissa J. BukowskiHollie JohnstonAlemu FiteSarita RaghunayakulaJohn KamholzLawrence I. GrossmanKarin PrzyklenkMaik HüttemannNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-12 (2018) |
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Medicine R Science Q Thomas H. Sanderson Joseph M. Wider Icksoo Lee Christian A. Reynolds Jenney Liu Bradley Lepore Reneé Tousignant Melissa J. Bukowski Hollie Johnston Alemu Fite Sarita Raghunayakula John Kamholz Lawrence I. Grossman Karin Przyklenk Maik Hüttemann Inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury |
description |
Abstract The interaction of light with biological tissue has been successfully utilized for multiple therapeutic purposes. Previous studies have suggested that near infrared light (NIR) enhances the activity of mitochondria by increasing cytochrome c oxidase (COX) activity, which we confirmed for 810 nm NIR. In contrast, scanning the NIR spectrum between 700 nm and 1000 nm revealed two NIR wavelengths (750 nm and 950 nm) that reduced the activity of isolated COX. COX-inhibitory wavelengths reduced mitochondrial respiration, reduced the mitochondrial membrane potential (ΔΨm), attenuated mitochondrial superoxide production, and attenuated neuronal death following oxygen glucose deprivation, whereas NIR that activates COX provided no benefit. We evaluated COX-inhibitory NIR as a potential therapy for cerebral reperfusion injury using a rat model of global brain ischemia. Untreated animals demonstrated an 86% loss of neurons in the CA1 hippocampus post-reperfusion whereas inhibitory NIR groups were robustly protected, with neuronal loss ranging from 11% to 35%. Moreover, neurologic function, assessed by radial arm maze performance, was preserved at control levels in rats treated with a combination of both COX-inhibitory NIR wavelengths. Taken together, our data suggest that COX-inhibitory NIR may be a viable non-pharmacologic and noninvasive therapy for the treatment of cerebral reperfusion injury. |
format |
article |
author |
Thomas H. Sanderson Joseph M. Wider Icksoo Lee Christian A. Reynolds Jenney Liu Bradley Lepore Reneé Tousignant Melissa J. Bukowski Hollie Johnston Alemu Fite Sarita Raghunayakula John Kamholz Lawrence I. Grossman Karin Przyklenk Maik Hüttemann |
author_facet |
Thomas H. Sanderson Joseph M. Wider Icksoo Lee Christian A. Reynolds Jenney Liu Bradley Lepore Reneé Tousignant Melissa J. Bukowski Hollie Johnston Alemu Fite Sarita Raghunayakula John Kamholz Lawrence I. Grossman Karin Przyklenk Maik Hüttemann |
author_sort |
Thomas H. Sanderson |
title |
Inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury |
title_short |
Inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury |
title_full |
Inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury |
title_fullStr |
Inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury |
title_full_unstemmed |
Inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury |
title_sort |
inhibitory modulation of cytochrome c oxidase activity with specific near-infrared light wavelengths attenuates brain ischemia/reperfusion injury |
publisher |
Nature Portfolio |
publishDate |
2018 |
url |
https://doaj.org/article/d38358554de345238b2771e0cebf73a7 |
work_keys_str_mv |
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