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Equipment, Education and Resources for Clinical Excellence in Energetic Therapies

Antioxidant Defense – Oxidative Stress

Photomed Laser Surg. 2010 Feb;28(1):23-30.

Biophoton detection and low-intensity light therapy: a potential clinical partnership.

Tafur J<>, Van Wijk EP<>, Van Wijk R<>, Mills PJ<>.

Department of Psychiatry, Behavioral Medicine Laboratory, University of California at San Diego, San Diego, CA, USA.jtafur@ucsd.edu

Abstract

Low-intensity light therapy (LILT) is showing promise in the treatment of a wide variety of medical conditions. Concurrently, our knowledge of LILT mechanisms continues to expand. We are now aware of LILT’s potential to induce cellular effects through, for example, accelerated ATP production and the mitigation of oxidative stress. In clinical use, however, it is often difficult to predict patient response to LILT. It appears that cellular reduction/oxidation (redox) state may play a central role in determining sensitivity to LILT and may help explain variability in patient responsiveness. In LILT, conditions associated with elevated reactive oxygen species (ROS) production, e.g. diabetic hyperglycemia, demonstrate increased sensitivity to LILT. Consequently, assessment of tissue redox conditions in vivo may prove helpful in identifying responsive tissues. A noninvasive redox measure may be useful in advancing investigation in LILT and may one day be helpful in better identifying responsive patients. The detection of biophotons, the production of which is associated with cellular redox state and the generation of ROS, represents just such an opportunity. In this review, we will present the case for pursuing further investigation into the potential clinical partnership between biophoton detection and LILT.

Aviakosm Ekolog Med. 2009 Jul-Aug;43(4):51-5.

Influence of infrared cold laser radiation emission on free radical processes in various tissues of rats with circulatory cerebral hypoxia

[Article in Russian]

Shurygina IP<>, Miliutina NP<>, Pokudina IO<>, Prokof’ev VN<>, Kussmaul’ AR<>, Shkurat TP<>.

Abstract

Influence of infrared cold laser emission (IRCL) on the dynamic equilibrium between lipid peroxidation and tension of the antioxidant defense system in rat’s tissues (blood, brain, retina, cornea) was evaluated in animals with circulatory cerebral hypoxia induced by occlusion of the left carotid artery. Tissues of white rats were examined for IRCL effects on hemiluminescence, malonic dialdehyde, SOD and catalase activities on the background of circulatory cerebral hypoxia. Data of the experiment evidenced an antioxidant effect of posthypoxic IRCL therapy as it reduces intensity of the free radical processes in plasma, cerebral tissues and retina. The experiment demonstrated the IRCL ability to modulate LPO, to stiffen the antioxidant defense system in the event of eye diseases originated from circulatory hypoxia of the ocular analyzer.

J Biochem Mol Toxicol. 2009 Jan;23(1):1-8.

Effects of low-level light therapy on hepatic antioxidant defense in acute and chronic diabetic rats.

Lim J<>, Ali ZM<>, Sanders RA<>, Snyder AC<>, Eells JT<>, Henshel DS<>, Watkins JB 3rd<>.

School of Public and Environmental Affairs, Indiana University, Bloomington, IN 47405, USA.

Abstract

Diabetes causes oxidative stress in the liver and other tissues prone to complications. Photobiomodulation by near infrared light (670 nm) has been shown to accelerate diabetic wound healing, improve recovery from oxidative injury in the kidney, and attenuate degeneration in retina and optic nerve. The present study tested the hypothesis that 670 nm photobiomodulation, a low-level light therapy, would attenuate oxidative stress and enhance the antioxidant protection system in the liver of a model of type I diabetes. Male Wistar rats were made diabetic with streptozotocin (50 mg/kg, ip) then exposed to 670 nm light (9 J/cm(2)) once per day for 18 days (acute) or 14 weeks (chronic). Livers were harvested, flash frozen, and then assayed for markers of oxidative stress. Light treatment was ineffective as an antioxidant therapy in chronic diabetes, but light treatment for 18 days in acutely diabetic rats resulted in the normalization of hepatic glutathione reductase and superoxide dismutase activities and a significant increase in glutathione peroxidase and glutathione-S transferase activities. The results of this study suggest that 670 nm photobiomodulation may reduce, at least in part, acute hepatic oxidative stress by enhancing the antioxidant defense system in the diabetic rat model.

Vopr Kurortol Fizioter Lech Fiz Kult. 2009 Jan-Feb;(1):17-9.

Parameters of lipid peroxidation and antioxidative protection in patients with chronic pancreatitis treated by low-intensity laser therapy

[Article in Russian]

Burduli NM<>, Gutnova SK<>.

Abstract

The objective of this study was to evaluate the influence of low-intensity laser therapy (LILT) on the processes of lipid peroxidation (LPO) and antioxidative protection (AOP) in patients with chronic pancreatitis. A total of 78 patients aged from 36 to 77 years were treated with LILT in addition to conventional therapy; the patients of the control group (n = 40) received only medicamentous therapy. Examination of the patients in the exacerbation phase of chronic pancreatitis revealed activation of LPO processes and differently-directed shifts of AOP components. These changes are supposed to reflect variations in the activity of the inflammatory processes in the pancreas and oxidative stress on this organ.

Photomed Laser Surg. 2008 Aug;26(4):323-8.

Low-intensity light therapy: exploring the role of redox mechanisms.

Tafur J<>, Mills PJ<>.

Department of Psychiatry, Behavioral Medicine Laboratory, University of California at San Diego, La Jolla, California 92093-0804, USA. jtafur@ucsd.edu

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.