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Avci et al. Page 7 efficacy following water exposure or perspiration, spectral limitations, possible toxic effects of nanoparticles that are contained by most sunscreens,60 user allergies, and compliance. It has recently been suggested that infrared (IR) exposure might have protective effects against UV-induced skin damage mainly by triggering protective/repair responses to UV irradiation. In the natural environment, visible and IR solar wavelengths predominate in the morning and UVB and UVA are maximal around noon which suggest that mammalians already possess a natural mechanism which, in reaction to morning IR radiation, prepares the skin for upcoming potentially damaging UV radiation at noon.61 However, opposing views also exist, such as Krutmann’s study demonstrating IR-induced disturbance of the electron flow of the mitochondrial electron transport chain which leads to inadequate energy production in dermal fibroblasts.62 Schroeder’s report is another example stating that IR alters the collagen equilibrium of the dermal extracellular matrix by leading to an increased expression of the collagen-degrading enzyme MMP-1, and by decreasing the de novo synthesis of the collagen itself.59 As previously mentioned, the same light source may have opposite effects on the same tissue depending on the parameters used and these conflicting views are probably due to the biphasic effects of light.18,19 Menezes et al. demonstrated that non-coherent near infrared radiation (NIR) (700–2,000 nm) generated a strong cellular defense against solar UV cytotoxicity in the absence of rising skin temperature and it was assumed to be a long-lasting (at least 24 hours) and cumulative phenomenon.63 Following this study, Frank et al. proposed that IR irradiation prepares cells to resist UVB-induced damage by affecting the mitochondrial apoptotic pathway.64 IR pre- irradiation of human fibroblasts was shown to inhibit UVB activation of caspase-9 and -3, partially release of cytochrome c and Smac/Diablo, decrease pro-apoptotic (ie, Bax) and increase anti-apoptotic proteins (ie, Bcl-2 or Bcl-xL).64 The results suggested that IR inhibited UVB-induced apoptosis by modulating the Bcl2/Bax balance, pointing to a role of p53, a sensor of gene integrity involved in cell apoptosis and repair mechanisms. In a further study, Frank et al. studied more specifically the role of the p53 cell signaling pathway in the prevention of UVB toxicity.64 The response to IR irradiation was shown to be p53 dependent which further suggests that IR irradiation prepares cells to resist and/or to repair further UVB-induced DNA damage. Finally, the IR induction of defense mechanisms was supported by Applegate et al. who reported that the protective protein, ferritin, normally involved in skin repair (scavenger of Fe2+ otherwise available for oxidative reactions) was induced by IR radiation.65 In an in vitro study, it was reported that an increase dermal fibroblast procollagen secretion reduces metalloproteinases (MMP) or collagenase production following non-thermal non- coherent deep red visible LED exposures (660 nm, sequential pulsing mode).40 These results correlated with significant clinical improvement of rhytids in vivo.40 In a subsequent in vivo pilot study, effect of this wavelength in 3 healthy subjects using a minimal erythemal dose (MED) method adapted from sunscreen SPF determination has been investigated.61 The results showed that LED therapy was effective, achieving a significant response in the reduction of the erythema induced by UVB.61 Following this pilot study a further investigation has been performed to find out in vivo aspects of this phenomenon. Effects of non-thermal, non-coherent 660 nm LED pulsed treatments in providing enhanced skin Semin Cutan Med Surg. Author manuscript; available in PMC 2014 August 08. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author ManuscriptPDF Image | Low-level laser (light) therapy (LLLT) in skin: stimulating, healing, restoring
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