Low-Intensity Light Therapy: Exploring the Role of Redox Mechanisms

Abstract

Low-intensity light therapy (LILT) appears to be working through newly recognized photoacceptor systems. The mitochondrial electron transport chain has been shown to be photosensitive to red and near-infrared (NIR) light. Although the underlying mechanisms have not yet been clearly elucidated, mitochondrial photostimulation has been shown to increase ATP production and cause transient increases in reactive oxygen species (ROS). In some cells, this process appears to participate in reduction/oxidation (redox) signaling. Redox mechanisms are known to be involved in cellular homeostasis and proliferative control. In plants, photostimulation of the analogous photosynthetic electron transport chain leads to redox signaling known to be integral to cellular function. In gene therapy research, ultraviolet lasers are being used to photostimulate cells through a process that also appears to involve redox signaling. It seems that visible and near visible low-intensity light can be used to modulate cellular physiology in some nonphotosynthetic cells, acting through existing redox mechanisms of cellular physiology. In this manner, LILT may act to promote proliferation and/or cellular homeostasis. Understanding the role of redox state and signaling in LILT may be useful in guiding future therapies, particularly in conditions associated with pro-oxidant conditions. 323

Low level laser therapy activates NF-kB via generation of reactive oxygen species in mouse embryonic fibroblasts

“…Reactive oxygen species (ROS) can both activate NF-kB directly [16], and ROS are also involved in NF-kB activation by other stimuli such as tumor necrosis factor alpha (TNFa), phorbol ester, and interleukin (IL)-1 [17]. Several laboratories have observed the formation of ROS in cells in vitro after LLLT [18,19,20,21], and it has been proposed that ROS are involved in the signaling pathways initiated after photons are absorbed by the mitochondria within cells [22].…”

Non‐thermal DNA damage of cancer cells using near‐infrared irradiation

“…(14) Actively proliferating cells also show increased sensitivity to red and NIR radiation. (12,13) The NIR spectrum of biological materials is a result of the overtones and combination of O-H, C-H, and N-H group bond stretching vibrations. (26) It is hypothesized that NIR mainly resonates helical structures, a-helices, and DNA.…”

“…(11) In addition, actively proliferating cells exhibit increased sensitivity to red and NIR wavelengths. (12,13) It appears that NIR irradiation induces DNA strand breaks and cell death by apoptosis, (14) and can elicit photodisruptive destruction of tumor tissue. (15) However, in-depth studies to date have not explored the optimal NIR wavelength that is most effective for treating cancer.…”

Non-Thermal Effects of Near-Infrared Irradiation on Melanoma

“…The penetrating 600-1300 nm wavelength region causes photochemical changes and affects a large volume and depth of tissue (Anderson & Parrish, 1981). Actively proliferating cells show increased sensitivity to red and NIR (Karu et al,1994;Tafur & Mills, 2008). NIR irradiation induces strand breaks and apoptosis (Tirlapur & König, 2001) as well as cell death of cancer cells and bone marrow cells (Tanaka et al, 2010b(Tanaka et al, , 2011b.…”

“…This may limit the possible uses of the 904 nm wavelength for certain body areas in races with skin that is rich in melanin. Actively proliferating cells show increased sensitivity to red and IR irradiation (Karu et al, 1994;Tafur & Mills, 2008). IR irradiation alone appears to induce DNA strand breaks and apoptosis (Tirlapur & König, 2001), which elicits photodisruptive destruction of tumor tissue (Dees et al, 2002).…”