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Dovepress Low-level light therapy physiology. Consistent with this idea, a number of intra- cellular effects have been described during and after light excitation. Based on these data, a mechanistic hypothesis on the mechanism of action of LLLT has been advanced. For study purposes, the mechanistic effects of LLLT can be divided into primary (during light exposure) and secondary (after light exposure). Primary effects Primary effects refer to the direct photochemical change occurring in the photoacceptor upon excitation by light. Primary effects are light-dependent and they occur only while the target tissue is being exposed to light. Current evi- dence is available to support at least three different primary effects. The first and most important primary effect is a redox change of the components of the respiratory chain. LLLT can induce reduction or oxidation of cytochrome oxidase. These changes in redox status correlate with the bell-shaped dose- response recorded for cellular responses.3 Changes in the redox status of cytochrome oxidase implicate alterations in electron flow. LLLT increases cytochrome c oxidation in the presence of cytochrome oxidase, causes increases in oxygen consumption and mitochondrial membrane potential, and activates the mitochondrial permeability transition pore.21,20 All of these events have been associated with accelerated electron flow in the mitochondrial electron transport chain. The second possible primary effect is the generation of free radicals, including singlet oxygen via direct photodynamic action and superoxide ion via one electron auto-oxidation. The significance of this effect is that reactive oxygen species are not only damaging by-products of respiration but they have an important role in cellular signaling. The third primary effect of LLLT is localized transient “heating” of the absorb- ing chromophore based on electric or light oscillations.21 This effect has been less characterized and it is believed to comple- ment the other two proposed primary effects. The effect of such oscillations appears to be more generalized and affect all molecules in the target tissue, including water. LLLT is able to strengthen hydrogen bonds and induce large-size hydrogen bonds networks that allow quick energy transfers due to resonant intermolecular energy transference. Thus, LLLT can cause nonequilibrium electrical fluctuations that bias Brownian motion and induce mechanisms that support electron pumping without heat transfer.14 Secondary effects The secondary effects of LLLT occur as a consequence of primary effects and include a cascade of biochemical Eye and Brain 2011:3 reactions that change cellular homeostasis.34,35 Secondary effects feature activation of second messengers with subse- quent modulation of enzyme function and gene expression. Secondary effects are distinctive because they can occur hours and even days after light exposure and they implicate the activation of signaling pathways that result in amplified macroeffects. Because they occur as part of cascade reactions, secondary effects tend to be pleiotropic. LLLT activates the retrograde signaling pathway from the mitochondria to the nucleus. This signaling pathway induces adaptive responses to stress by sending information from mitochondria, which contain the photoacceptors, to the nucleus, which can then respond by altering levels of gene expression. The initial phase of this pathway has been proposed to be an increase in the NAD/NADH ratio and mitochondrial intermembrane potential, dissociation of nitric oxide from its binding site in cytochrome oxidase, and modification of the ATP pool. Even small changes in ATP alter cellular metabolism. ATP acti- vates P2 receptors (P2X and P2Y) to induce inward calcium currents and release of calcium from intracellular stores.35 Changes in ATP also alter cyclic adenosine monophosphate levels, with subsequent activation of kinases. Downstream consequences of these secondary effects involve changes in gene expression, which impact mitogenic signaling, surface molecule expression, and expression of proteins regulating inflammatory, redox states, and apoptosis (Figure 5). Effects of LLLT on nervous tissue A growing body of evidence supports an enhancing or pro- tective role of LLLT in nervous tissue. Neurons are highly specialized cells with a major dependence on sustained aero- bic energy production. Mitochondrial aerobic metabolism in neurons is the basis for electrophysiological, neuroplastic, and neuroprotective functions including repolarization of cell membranes in neurotransmission, synapse formation, and cell survival. At a large scale, energy metabolism is also crucial for adequate function of neuronal networks, data integration in space and time, and sensory processing including vision, activation of motor function, and expression of higher-order cognitive functions such as memory. It has been demonstrated that impaired mitochondrial oxidative metabolism is associated with neuronal dysfunction, neu- rological impairment, and neurodegeneration.36 Therefore, interventions aimed at improving mitochondrial metabolism are hypothesized to benefit the function of both the diseased and normal brain. Recent studies have confirmed that the effects of LLLT on nervous tissue are also mediated at least in part by submit your manuscript | www.dovepress.com Dovepress 57PDF Image | Low-level light therapy of the eye and brain
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