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Low‐level laser therapy (LLLT) reduces oxidative stress in primary cortical neurons in vitro
Author(s) -
Huang YingYing,
Nagata Kazuya,
Tedford Clark E.,
McCarthy Thomas,
Hamblin Michael R.
Publication year - 2013
Publication title -
journal of biophotonics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.877
H-Index - 66
eISSN - 1864-0648
pISSN - 1864-063X
DOI - 10.1002/jbio.201200157
Subject(s) - reactive oxygen species , oxidative stress , viability assay , mitochondrion , chemistry , membrane potential , in vitro , rotenone , low level laser therapy , microbiology and biotechnology , mitochondrial ros , biology , biochemistry , laser therapy , laser , physics , optics
L ow‐ l evel l aser (light) therapy (LLLT) involves absorption of photons being in the mitochondria of cells leading to improvement in electron transport, increased mitochondrial membrane potential (MMP), and greater ATP production. Low levels of reactive oxygen species (ROS) are produced by LLLT in normal cells that are beneficial. We exposed primary cultured murine cortical neurons to oxidative stressors: hydrogen peroxide, cobalt chloride and rotenone in the presence or absence of LLLT (3 J/cm 2 , CW, 810 nm wavelength laser, 20 mW/cm 2 ). Cell viability was determined by Prestoblue TM assay. ROS in mitochondria was detected using Mito‐sox, while ROS in cytoplasm was detected with CellRox TM . MMP was measured with tetramethylrhodamine. In normal neurons LLLT elevated MMP and increased ROS. In oxidatively‐stressed cells LLLT increased MMP but reduced high ROS levels and protected cultured cortical neurons from death. Although LLLT increases ROS in normal neurons, it reduces ROS in oxidatively‐stressed neurons. In both cases MMP is increased. These data may explain how LLLT can reduce clinical oxidative stress in various lesions while increasing ROS in cells in vitro. (© 2013 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)