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Rojas and Gonzalez-Lima Dovepress Protective effects were observed when striatal and cortical rat neuronal cultures were exposed to rotenone and 1-methyl- 4-phenylpyridinium (MPP+) toxins that inhibit mitochondrial complex I. LLLT significantly increased cellular ATP con- tent, decreased the number of neurons undergoing cell death, and reduced the expressions of reactive oxygen species and reactive nitrogen species in rotenone- or MPP+-exposed neurons as compared with untreated ones.41 Furthermore prophylactic LLLT in vitro has proved very effective at protecting neurons from neurodegeneration induced by mitochondrial toxins.9,36,38,40 Notably, LLLT pretreatment suppresses rotenone- or MPP+-induced apoptosis in both striatal and cortical neurons.38 LLLT has been also suc- cessfully employed for nerve repair and reduction of neural injury in animal models,42 and it is clinically used to relieve pain in humans.43 A number of secondary effects of LLLT on nervous tissue have also been described, including: (1) increased expression of the anti-apoptotic protein Bcl-2 and reduced expression of the proapoptotic protein Bax,38 (2) decreased numbers of apoptotic cells after exposure to the amyloid beta protein,44 (3) improved function of cortical neurons inactivated by toxins,9,38 (4) increased survival and ATP content of striatal neurons after rotenone- and MPP+-induced toxicity and decreased oxidative stress and nitric oxide production,40 (5) increased neurite outgrowth,45 (6) regulation of genes encoding for DNA repair proteins, antioxidant enzymes, and molecular chaperones,8 and (7) increased proliferation of olfactory ensheating stem cells,39 Schwann cells,46 astrocytes, and oligodendrocytes.47 In vivo, LLLT induces peripheral and central nerve regeneration after trauma,42,47,48 reduces neuroinflammation,42 prevents methanol-induced photore- ceptor degeneration,12 and prevents retinal neurodegeneration induced by complex I inhibition.49 Beneficial in vivo effects of LLLT in the eye Light tissue penetration depends on both the type of target tis- sue, wavelength, and the source of LLLT (Figure 2). Besides being safe, at near-infrared wavelengths, light penetration to the eye is maximal, where absorption by the cornea and lens is negligible (,10%) and high refractive indices favor low light scattering and a high degree of focusing on the retina.50 The retina contains neurons with extremely high energy demands that rely mostly on mitochondrial-derived ATP to meet these requirements.51–53 Mitochondria play a central role in neuronal physiology. These organelles integrate cell respiration, energy metabolism, and ionic balance into a Eye and Brain 2011:3 LLLT Cytochrome oxidase redox change Preservation of neuronal structure and function Improved visual function Improved motor function Improved cognitive function Figure 5 The intracellular mechanisms of action of low-level light therapy (LLLT). Photobiomodulation results in a cascade of intracellular pleiotropic effects. Light is absorbed by chromophores in cytochrome oxidase and induces changes in its redox state. Redox reaction of enzymes in the inner mitochondrial membrane induces accelerated electron flow, reduced nicotine adenine dinucleotide (NADH) consumption and increase in the mitochondrial membrane potential. These changes facilitate the synthesis of adenosine triphosphate (ATP) and increase the generation of free radicals. increased ATP availability allows the activation of kinases that induce the release of calcium and the formation of cyclic adenosine monophosphate (cAMP). Calcium, cAMP, and free radicals act as second messengers and are able to activate different metabolic pathways at the nuclear level. Depending on the cell environment, these cellular changes can be adaptive and promote enhancement of neuronal physiology that translates in clinical improvement. enhancement of cytochrome oxidase activity. Rat neuronal cultures exposed to LLLT showed increases in cytochrome oxidase activity.9 These increases of cytochrome oxidase induced by LLLT parallel those observed in other tissues with high metabolic demands such as muscle.37 A similar enhancing effect of LLLT was also observed when deliv- ered after exposure of neurons in culture to tetradotoxin, which blocks electrical neural activity and indirectly inhibits cytochrome oxidase activity.38 In addition, LLLT partially restored enzyme activity blocked by potassium cyanide, a cytochrome oxidase inhibitor, and significantly reduced neuronal cell death.9 This illustrates that the enhancing effects of LLLT on neuronal metabolism are not limited to enhancement of cytochrome oxidase activity, but have the potential to exert extended effects such as enhancement of ATP production,36 neurotransmission,8 gene expression,38,39 and prevention of cell death in vitro.40,41 58 submit your manuscript | www.dovepress.com Dovepress NAD-NADH ratio Mitochondrial membrane potential ATP Free radicals Calcium release cAMP Gene expression Mitogenic signals Surface molecule expression Inflammation Apoptosis Energy metabolismPDF Image | Low-level light therapy of the eye and brain
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