It has been known for many years that low levels of laser or non-coherent light in the red or near-infrared spectrum (LLLT) accelerate some phases of wound healing, but the benefits of LLLT in wound healing and medicine in general are still controversial. Partly this may be explained by the complicated dosimetry that pertains with regard to coherence, monochromaticity, wavelength, total fluence, pulse-structure, polarization state, power density and treatment repetition. However, another major reason for the non-acceptance by the general medical community is the widespread uncertainty about the molecular, cellular and tissue mechanisms that transduce signals from the incident photons via chromophores and signaling pathways to the observed biological effects.
We have been investigating these events and have discovered that a likely mechanism that applies in LLLT involves alteration of mitochondrial respiration that both increases cellular ATP levels and at the same time produces intracellular reactive oxygen species (ROS). We believe that these ROS activate cellular pathways designed to cope with low levels of oxidative stress. Redox-sensitive transcription factors such as NF-kB are activated, leading to expression of an array of gene products that prevent apoptosis and cell death, stimulate fibroblast proliferation, migration and collagen synthesis, modulate the inflammatory and anti-oxidant response, and stimulate angiogenesis and tissue repair.
Neuronal cells respond well to LLLT due to their high mitochondrial activity and we have shown that in vitro LLLT has a biphasic dose response, whereby a small amount of light is beneficial while a large amount of light loses the benefit and can be harmful. We have shown that LLLT can protect cultured cortical neurons from oxidative stress and from excitotoxicity.
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