The use of low levels of visible or near infrared light for reducing pain, inflammation and edema, promoting healing of wounds, deeper tissues and nerves, and preventing cell death and tissue damage has been known for over forty years. Despite many reports of positive findings from experiments conducted in vitro, in animal models and in randomized controlled clinical trials, LED phototherapy remains controversial in mainstream medicine due to incomplete understanding of the basic mechanisms and the selection of inappropriate dosimetric parameters that led to negative studies. In LED phototherapy, the question is no longer whether light has biological effects but rather how light from therapeutic LEDs works at the cellular and organism levels and what the optimal light parameters are for different uses of these light sources.
Mechanisms of low level light therapy
According to the First Law of Photochemistry, the photons of light must be absorbed by some molecular photoacceptors or chromophores for photochemistry to occur (Sutherland 2002). The mechanism of Low level light therapy (LLLT) at the cellular level has been attributed to the absorption of monochromatic visible and near infrared (NIR) radiation by components of the cellular respiratory chain (Karu 1989). Phototherapy is characterized by its ability to induce photobiological processes in cells. The effective tissue penetration of light and the specific wavelength of light absorbed by photoacceptors are two of the major parameters to be considered in light therapy. In tissue there is an “optical window” that runs approximately from 650 nm to 1200 nm where the effective tissue penetration of light is maximized. Therefore the use of LLLT in animals and patients almost exclusively involves red and near-infrared light (600-1100-nm) (Karu and Afanas’eva 1995).
Mitochondria play an important role in energy generation and metabolism and are involved in current research about the mechanism of LLLT effects. The absorption of monochromatic visible and NIR radiation by components of the cellular respiratory chain has been considered as the primary mechanism of LLLT at the cellular level (Karu 1989).
Light is initially absorbed by mitochondrial chromophore or photoacceptor, cytochrome C oxidase (CCO) and causes increased production of ATP and reactive oxygen species (ROS) and release of nitric oxide (NO), which, in turn, cause changes in cellular redox potential, Ca2+, K+, cAMP, and pH levels and induce several transcription factors (AP–1, NFkB, HIF-1α) concerned with cell proliferation, survival, and tissue repair and regeneration (Handbook of Photomedicine).
Why ATP is so important for human body
(Nina Mikirova, Ph.D.;Hugh D. Riordan, M.D.;R.K. Kirby, M.D.;A. Klykov, B.S.;James A. Jackson, Ph.D., Monitoring of ATP Levels in Red Blood Cells and T Cells of Healthy and ill Subjects and the Effects of Age on Mitochondrial Potential, The Bio-Communications Research Institute, Inc., 3100 N. Hillside Avenue, Wichita KS, 67219,)
Adenosine triphosphate (ATP) is at the root of all organisms energetics. ATP provides the energetics for all muscle movements, heart beats, nerve signals and chemical reactions inside the body. It is estimated that the human body uses roughly 2 × 1026 transient molecules of ATP or more than the bodies weight; 160 kg of ATP in a day. ATP stores energy in a high energy phosphate bond, the third phosphate bond. The cutting of one phosphate bond, ATP + H2O → ADP + Pi liberates about 30.6 kJ/mole.
Energy metabolism plays a role in health and aging as well as disease. Energy must be available for the work of synthesizing new cellular material, maintaining membranes and organelles, and to fuel movement and active transport. Determination of the concentration of the energy carrier molecule, adenosine-5′-triphosphate (ATP), may assess the energy state in cells. Cellular ATP is an important determinant of cell death by apoptosis or necrosis. Cells stay alive as long as a certain level of ATP is maintained. When ATP falls below this level, apoptosis is activated. A severe drop in cellular ATP will result in cellular necrosis. Metabolic conditions such as, trauma or stress may increase requirements for ATP or reduce the regeneration of ATP, therefore decreasing the overall ATP available to the body. Several pathological conditions may also decrease ATP production in cells. In addition, age and age-related diseases may be due to a fall in energy metabolism in the mitochondria. For example, patients with chronic fatigue syndrome (CFS) have relatively low intracellular ATP concentrations after exercise and a lower ATP synthesis rate during recovery. In type II diabetes, alterations in the ATP synthesis may contribute to the pathogenesis of this disease. Lower ATP levels, number of hemoglobin and RBC deficiencies are common in cancer patients. The cellular level of ATP in subjects with solid tumors may be 30 % lower than that of normal adults.
Pathological conditions may have an influence on the ATP content. Levels of ATP in T cells was found to be lower in patients with breast, prostate, colon, and lung cancer, as well as in patients with anemia and thyroid disorder. The lower level of ATP in T cells of these patients indicates a lower host defense capability, as the T lymphocytes are important cellular components of the immune system. T cells can both modulate the function of other immune cells and directly destroy cells infected with intracellular pathogens.
Results of the analysis allowed important conclusions about the dependence of mitochondrial potential on age and decline in potential with age. This effect may result from age-associated accumulation of mitochondrial defects due to oxidative damage, as these defects are the major contributors to cellular, tissue and organism aging.
Mitochondria are implicated in the aging of cells. This is supported by the fact that these organelles are both responsible for most of energy production and for generation of free radicals by the electron transport chain. The age-related alterations in respiration, ATP synthesis, ADP/ATP translocation are found in mitochondria with age. The most important mitochondrial changes are age-related irreversible damage to mitochondrial DNA (mtDNA) by free radicals. The lack of a mtDNA repair mechanism leads to accumulation of errors and increases in gene mutations. Continuous accumulation of mutations may lead to deterioration in oxidative phosphorylation and further decline in energy production.