Low level laser therapy reduces oxidative stress in cortical neurons in vitro

Ying Ying Huang; Clark E. Tedford; Thomas McCarthy; Michael R. Hamblin

doi:10.1117/12.912948

Low level laser therapy reduces oxidative stress in cortical neurons in vitro

Ying Ying Huang, Clark E. Tedford, Thomas McCarthy, Michael R. Hamblin

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

Abstract

It is accepted that the mechanisms of low level laser therapy (LLLT) involves photons that are absorbed in the mitochondria of cells and lead to increase of mitochondrial metabolism resulting in more electron transport, increase of mitochondrial membrane potential, and more ATP production. Intracellular calcium changes are seen that correlate with mitochondrial stimulation. The situation with two other intermediates is more complex however: reactive oxygen species (ROS) and nitric oxide (NO). Evidence exists that low levels of ROS are produced by LLLT in normal cells that can be beneficial by (for instance) activating NF-kB. However high fluences of light can produce large amounts of ROS that can damage the cells. In oxidatively stressed cells the situation may be different. We exposed primary cultured cortical neurons to hydrogen peroxide (H ₂O ₂) or cobalt chloride (CoCl ₂) oxidative insults in the presence or absence of LLLT (810-nm laser at 0.3 or 3 J/cm ²). Cell viability of cortical neurons was determined by lactate dehydrogenase assay. ROS in neurons was detected using an ROS probe, MitoRox with confocal microscopy. Results showed that LLLT dose-dependently reversed ROS production and protected cortical neurons against H ₂O ₂ or CoCl ₂ induced oxidative injury in cultured cortical neurons. Conclusion: LLLT can protect cortical neurons against oxidative stress by reversing the levels of ROS.

Original language	English
Title of host publication	Mechanisms for Low-Light Therapy VII
DOIs	https://doi.org/10.1117/12.912948
Publication status	Published - 2012
Externally published	Yes
Event	Mechanisms for Low-Light Therapy VII - San Francisco, CA, United States Duration: 21 Jan 2012 → 21 Jan 2012

Publication series

Name	Progress in Biomedical Optics and Imaging - Proceedings of SPIE
Volume	8211
ISSN (Print)	1605-7422

Conference

Conference	Mechanisms for Low-Light Therapy VII
Country/Territory	United States
City	San Francisco, CA
Period	21/01/12 → 21/01/12

Keywords

Cobalt chloride
Cultured cortical neurons
Hydrogen peroxide
Low-level laser therapy
Oxidative stress
Reactive oxygen species

ASJC Scopus subject areas

Electronic, Optical and Magnetic Materials
Biomaterials
Atomic and Molecular Physics, and Optics
Radiology, Nuclear Medicine and Imaging

Access to Document

10.1117/12.912948

Cite this

@inproceedings{80162b4c3fc14b08a57c388ed1d61b9d,

title = "Low level laser therapy reduces oxidative stress in cortical neurons in vitro",

abstract = "It is accepted that the mechanisms of low level laser therapy (LLLT) involves photons that are absorbed in the mitochondria of cells and lead to increase of mitochondrial metabolism resulting in more electron transport, increase of mitochondrial membrane potential, and more ATP production. Intracellular calcium changes are seen that correlate with mitochondrial stimulation. The situation with two other intermediates is more complex however: reactive oxygen species (ROS) and nitric oxide (NO). Evidence exists that low levels of ROS are produced by LLLT in normal cells that can be beneficial by (for instance) activating NF-kB. However high fluences of light can produce large amounts of ROS that can damage the cells. In oxidatively stressed cells the situation may be different. We exposed primary cultured cortical neurons to hydrogen peroxide (H 2O 2) or cobalt chloride (CoCl 2) oxidative insults in the presence or absence of LLLT (810-nm laser at 0.3 or 3 J/cm 2). Cell viability of cortical neurons was determined by lactate dehydrogenase assay. ROS in neurons was detected using an ROS probe, MitoRox with confocal microscopy. Results showed that LLLT dose-dependently reversed ROS production and protected cortical neurons against H 2O 2 or CoCl 2 induced oxidative injury in cultured cortical neurons. Conclusion: LLLT can protect cortical neurons against oxidative stress by reversing the levels of ROS.",

keywords = "Cobalt chloride, Cultured cortical neurons, Hydrogen peroxide, Low-level laser therapy, Oxidative stress, Reactive oxygen species",

author = "Huang, {Ying Ying} and Tedford, {Clark E.} and Thomas McCarthy and Hamblin, {Michael R.}",

year = "2012",

doi = "10.1117/12.912948",

language = "English",

isbn = "9780819488541",

series = "Progress in Biomedical Optics and Imaging - Proceedings of SPIE",

booktitle = "Mechanisms for Low-Light Therapy VII",

note = "Mechanisms for Low-Light Therapy VII ; Conference date: 21-01-2012 Through 21-01-2012",

}

Huang, YY, Tedford, CE, McCarthy, T & Hamblin, MR 2012, Low level laser therapy reduces oxidative stress in cortical neurons in vitro. in Mechanisms for Low-Light Therapy VII., 821103, Progress in Biomedical Optics and Imaging - Proceedings of SPIE, vol. 8211, Mechanisms for Low-Light Therapy VII, San Francisco, CA, United States, 21/01/12. https://doi.org/10.1117/12.912948

Low level laser therapy reduces oxidative stress in cortical neurons in vitro. / Huang, Ying Ying; Tedford, Clark E.; McCarthy, Thomas et al.
Mechanisms for Low-Light Therapy VII. 2012. 821103 (Progress in Biomedical Optics and Imaging - Proceedings of SPIE; Vol. 8211).

Research output: Chapter in Book/Report/Conference proceeding › Conference contribution › peer-review

TY - GEN

T1 - Low level laser therapy reduces oxidative stress in cortical neurons in vitro

AU - Huang, Ying Ying

AU - Tedford, Clark E.

AU - McCarthy, Thomas

AU - Hamblin, Michael R.

PY - 2012

Y1 - 2012

N2 - It is accepted that the mechanisms of low level laser therapy (LLLT) involves photons that are absorbed in the mitochondria of cells and lead to increase of mitochondrial metabolism resulting in more electron transport, increase of mitochondrial membrane potential, and more ATP production. Intracellular calcium changes are seen that correlate with mitochondrial stimulation. The situation with two other intermediates is more complex however: reactive oxygen species (ROS) and nitric oxide (NO). Evidence exists that low levels of ROS are produced by LLLT in normal cells that can be beneficial by (for instance) activating NF-kB. However high fluences of light can produce large amounts of ROS that can damage the cells. In oxidatively stressed cells the situation may be different. We exposed primary cultured cortical neurons to hydrogen peroxide (H 2O 2) or cobalt chloride (CoCl 2) oxidative insults in the presence or absence of LLLT (810-nm laser at 0.3 or 3 J/cm 2). Cell viability of cortical neurons was determined by lactate dehydrogenase assay. ROS in neurons was detected using an ROS probe, MitoRox with confocal microscopy. Results showed that LLLT dose-dependently reversed ROS production and protected cortical neurons against H 2O 2 or CoCl 2 induced oxidative injury in cultured cortical neurons. Conclusion: LLLT can protect cortical neurons against oxidative stress by reversing the levels of ROS.

AB - It is accepted that the mechanisms of low level laser therapy (LLLT) involves photons that are absorbed in the mitochondria of cells and lead to increase of mitochondrial metabolism resulting in more electron transport, increase of mitochondrial membrane potential, and more ATP production. Intracellular calcium changes are seen that correlate with mitochondrial stimulation. The situation with two other intermediates is more complex however: reactive oxygen species (ROS) and nitric oxide (NO). Evidence exists that low levels of ROS are produced by LLLT in normal cells that can be beneficial by (for instance) activating NF-kB. However high fluences of light can produce large amounts of ROS that can damage the cells. In oxidatively stressed cells the situation may be different. We exposed primary cultured cortical neurons to hydrogen peroxide (H 2O 2) or cobalt chloride (CoCl 2) oxidative insults in the presence or absence of LLLT (810-nm laser at 0.3 or 3 J/cm 2). Cell viability of cortical neurons was determined by lactate dehydrogenase assay. ROS in neurons was detected using an ROS probe, MitoRox with confocal microscopy. Results showed that LLLT dose-dependently reversed ROS production and protected cortical neurons against H 2O 2 or CoCl 2 induced oxidative injury in cultured cortical neurons. Conclusion: LLLT can protect cortical neurons against oxidative stress by reversing the levels of ROS.

KW - Cobalt chloride

KW - Cultured cortical neurons

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KW - Low-level laser therapy

KW - Oxidative stress

KW - Reactive oxygen species

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SN - 9780819488541

T3 - Progress in Biomedical Optics and Imaging - Proceedings of SPIE

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ER -

Low level laser therapy reduces oxidative stress in cortical neurons in vitro

Abstract

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Conference

Keywords

ASJC Scopus subject areas

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