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Biphasic dose response in low level light therapy like 50 or 100 J/cm2 will lose the beneficial effect and may even become detrimental. The molecular and cellular mechanisms LLLT suggest that photons are absorbed by the mitochondria; they stimulate more ATP pro- duction and low levels of ROS, which then activates transcription factors, such as NF-κB, to induce many gene transcript products responsible for the beneficial effects of LLLT. ROS are well known to stimulate cellular proliferation of low levels, but inhibit proliferation and kill cells at high levels. Nitric oxide is also involved in LLLT, and may be photo-released from its binding sites in the respiratory chain and elsewhere. It is possible that NO release in low amounts by low dose light may be beneficial, while high levels released by high dose LLLT may be damaging. The third pos- sibility is that LLLT may activate transcription factors, upregulating pro- tective proteins which are anti-apoptotic, and generally promote cell sur- vival. In contrast, it is entirely possible that different transcription factors and cell-signaling pathways, that promote apoptosis, could be activated after higher light exposure. We believe that further advances in the mech- anistic understanding of LLLT will continue to be made in the near future. These advances will lead to greater acceptance of LLLT in main- stream medicine and may lead to LLLT being used for serious diseases such as stroke, heart attack and degenerative brain diseases. Nevertheless the concept of biphasic dose response or LLLT hormesis (low levels of light are good for you, while high levels are bad for you) will remain. ACKNOWLEDGMENTS Research in the Hamblin laboratory is supported by the US NIH (grants R01CA/AI838801 and R01AI050875 to MRH). REFERENCES Ad N and Oron U. 2001. Impact of low level laser irradiation on infarct size in the rat following myocardial infarction. Int J Cardiol 80:109-16. Agaiby AD, Ghali LR, Wilson R, and Dyson M. 2000. Laser modulation of angiogenic factor produc- tion by T-lymphocytes. Lasers Surg Med 26:357-63. Aimbire F, Albertini R, Pacheco MT, Castro-Faria-Neto HC, Leonardo PS, Iversen VV, Lopes-Martins RA, and Bjordal JM. 2006. Low-level laser therapy induces dose-dependent reduction of TNFalpha levels in acute inflammation. Photomed Laser Surg 24:33-7. al-Watban FA and Andres BL. 2001. The effect of He-Ne laser (632.8 nm) and Solcoseryl in vitro. Lasers Med Sci 16:267-75. Alexandratou E, Yova D, Handris P, Kletsas D, and Loukas S. 2002. Human fibroblast alterations induced by low power laser irradiation at the single cell level using confocal microscopy. Photochem Photobiol Sci 1:547-52. Anders J, Romanczyk T, Moges H, Ilev I, Waynant R, and Longo L. 2007. Light Interaction With Human Central Nervous System Progenitor Cells. NAALT conference proceedings. 2007 Anggard E. 1994. Nitric oxide: mediator, murderer, and medicine. Lancet 343:1199-206. Basford JR, Sheffield CG, and Harmsen WS. 1999. Laser therapy: a randomized, controlled trial of the effects of low-intensity Nd:YAG laser irradiation on musculoskeletal back pain. Arch Phys Med Rehabil 80:647-52. Bertolucci LE and Grey T. 1995. Clinical analysis of mid-laser versus placebo treatment of arthralgic TMJ degenerative joints. Cranio 13:26-9.PDF Image | BIPHASIC DOSE RESPONSE IN LOW LEVEL LIGHT THERAPY
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