Role of reactive oxygen species in low level light therapy

Abstract

This review will focus on the role of reactive oxygen species in the cellular and tissue effects of low level light therapy (LLLT). Coincidentally with the increase in electron transport and in ATP, there has also been observed by intracellular fluorescent probes and electron spin resonance an increase in intracellular reactive oxygen species (ROS) such as superoxide, hydrogen peroxide, singlet oxygen and hydroxyl radical. ROS scavengers, antioxidants and ROS quenchers block many LLLT processes. It has been proposed that light between 400-500-nm may produce ROS by a photosensitization process involving flavins, while longer wavelengths may directly produce ROS from the mitochondria. Several redox-sensitive transcription factors are known such as NF-kB and AP1, that are able to initiate transcription of genes involved in protective responses to oxidative stress. It may be the case that LLLT can be pro-oxidant in the short-term, but anti-oxidant in the long-term.

Transcranial LED therapy for cognitive dysfunction in chronic, mild traumatic brain injury: two case reports

“…During LLLT, absorption of red or NIR photons by cytochrome c oxidase in the mitochondrial respiratory chain [42] causes an increase in cellular respiration that continues for much longer than the light is present when delivered at appropriate fluence and exposure durations. Primary cellular effects include increase in mitochondrial respiration [43] , increase in ATP synthesis [43][44][45] , production of low levels of reactive oxygen species (ROS) [46] , modulate expression of 111 genes in a cDNA microarray study [47] , and increase nerve cell proliferation and migration [48] . Transcranial NIR light that penetrates the scalp and skull, can significantly reduce damage from experimentally induced stroke in rats [48] and rabbits [49] , can improve the memory performance of middle aged mice [50] , and has been shown to reduce damage from acute stroke in humans [51,52] .…”

Low-level laser therapy (904nm) can increase collagen and reduce oxidative and nitrosative stress in diabetic wounded mouse skin

“…The basic biological mechanism behind the effects of LLLT is thought to be via absorption of red and infra red light by cytochrome c oxidase (complex IV of the mitochondrial respiratory chain) [7]. In addition, Karu [8] and other authors [9] have proposed that one of the possible mechanisms of action of LLLT, is a brief and modest increase in production of ROS such as superoxide (O 2− ) and hydrogen peroxide (H 2 O 2 ), leading to restoration of the redox imbalance as a consequence of enhanced production of antioxidant enzymes. LLLT alters the redox state in cells and can induce the activation of intracellular signaling, increase activation of redox-sensitive transcription factors [10], and affect enzyme activation and cell cycle progression [7] which are fundamental mechanisms involved in wound healing.…”

Two-photon fluorescence imaging of intracellular hydrogen peroxide with chemoselective fluorescent probes

“…[10][11][12] In addition, H 2 O 2 is involved in therapeutic processes such as wound healing, stem cell proliferation, and an adaptive response in astrocytes leading to neuronal protection. 1,2,7,13 A substantial challenge in elucidating the diverse roles of H 2 O 2 in complex biological environments is the lack of methods to determine the spatial and temporal dynamics of this reactive oxygen metabolite in living systems. For the detection of ROS production in vitro, several fluorescent probes have been developed based on small molecules, fluorescent proteins, and nanoparticles.…”