PDF Publication Title:
Text from PDF Page: 007
Figure 8. Assessment of the organ weights and lung pathology of rats exposed to either OIR, 670nm or both. There was no change in the weights of animals exposed to 670nm from control (A). The OIR animals showed a statistically significant decrease in organ weight in both the kidneys and liver (* indicates p <0.05). There was an increase in the number of lung pathology (B) presentations (both haemorrhages and oedema) in the OIR exposed animals. This was ameliorated by 670nm exposure compared to control levels. 670nm alone showed no change from control levels. 670nm treated OIR animals did not show any difference from OIR levels. OIR – Oxygen Induced Retinopathy. Graph bar fills indicate controls (black), 670nm treated (dark grey), OIR (light grey) and 670nm+OIR (white). doi: 10.1371/journal.pone.0072135.g008 and increasing ATP production [37,38]. This hs been shown in number of non-neuronal cells, such as astrocytes [39] and fibroblast [40] however has been most effective in CNS tissue (reviewed in 36). This is probably due to the high metabolic demands of neuronal tissue, and subsequent susceptibility to damage as a result of fluctuations in oxidative metabolism. In these OIR models it is possible that 670nm red light promotes consumption of the excess oxygen available in the hyperoxic phase of the disease, making oxygen levels in the tissues closer to normoxia, and facilitating more normal development of the retinal vasculature. Establishing normoxia in the retinal microenvironment implies a moderation of the oxidative stress conditions that result from hyperoxia. Indeed recent experiments show that in adult mice exposed to hyperoxia, levels of acrolein and haemoxygenase, both markers of oxidative stress, are significantly reduced in the retina by exposure to 670nm red light (Albarracin, manuscript in preparation). A reduction in oxidative stress may also explain reduced natural cell death in the retina, and could minimise damage [9] to organs susceptible to fluctuations in oxygen levels, including the lungs. While the present results support this hypothesis, more work is required to understand the mechanism/s of action of 670nm red light. An alternative hypothesis is that neuroglia cells, including astrocytes, which are damaged by OIR experimental conditions [41] are protected by 670nm red light exposure during the hyperoxic phase, preserving normal processes of vascular development. This idea is consistent with previous findings that 670nm red light exposure moderates the expression of inflammatory markers and complement in retinal degeneration induced by bright light [42]. Finally, photoreceptor dysfunction and retinal cell death have been reported in OIR animal models [43] and in ROP [44]. Neuroprotection is therefore an important aspect for evaluation of ROP treatment and management. This study shows that the neural retina, and specifically the photoreceptors, are protected from cell death and OIR by 670nm red light therapy. Such protection of photoreceptors is consistent with other models, including the rodent light damage model [45], indicating that oxidative damage is a common feature in photoreceptor death [15,16,19]. Excessive white light [45] and certain wavelengths of light [46] have been shown to be toxic to photoreceptors, however there is no evidence to suggest 670nm is damaging to photoreceptors [15,16,18,19,42]. This is possibly due to the mechanisms of phototoxicity and photobiomodulation being different with white light acting on the photopigments, leading to lipid peroxidation and oxidative stress [47] and 670nm red light acting on the cytochrome c oxidase promoting efficient mitochondrial function. Although not the focus of this study our findings indicate that 670nm treatment may be beneficial in the management of other complications of prematurity, in particular Chronic Lung Disease (CLD). Hyperoxic and hypoxic states also influence the development of CLD [48], which in turn contributes to vulnerability to ROP because of the fluctuations in arterial oxygenation related to the lung disease and oxygen treatment required to maintain normal saturations. It is possible that 670nm red light may reduce the severity of CLD, by reducing inflammation and stabilising lung development and alveolarisation during hyperoxia, resulting in more ordered vascular development, and fewer haemorrhages. Systemic changes to inflammation have been described in a recent study [49] where inflammatory markers were modulated following low-level-laser therapy (660nm) treatment in an animal model of heart failure. This study supports these previous findings that systemic changes to biology, and specifically inflammation, can occur from localised LLLT and presents the first indication that 670nm red light can protect the lungs from CLD. Indeed, we suggest that such a decrease in inflammation and increase in metabolic efficiency explains the decreased mortality of mice treated with 670nm red light. However, further work is required to document the influences of 670nm red light on lung development and neonatal survival. Conclusion As modern-medicine pushes the survivability limits of pre- term babies, we must endeavour to find solutions to the complicated problems associated with lower preterm survivability, such as the increased incidence and severity of ROP. Exposure to 670nm red light is a potential novel, non- invasive and inexpensive treatment for the prevention and moderation of ROP. Acknowledgements We wish to thank Ms Kirsti Harrington (Anatomical Pathology, ACT Pathology, The Canberra Hospital) for her technical assistance in processing, sectioning and staining the tissues used in the histological assessment of organs and to Mr Keith PLOS ONE | www.plosone.org 7 August 2013 | Volume 8 | Issue 8 | e72135 670nm Protects against Retinopathy of PrematurityPDF Image | 670nm Photobiomodulation as a Novel Protection to Retinopathy
PDF Search Title:
670nm Photobiomodulation as a Novel Protection to RetinopathyOriginal File Name Searched:
05f0c1a1f2e8aec2744443e83bbeec817202.pdfDIY PDF Search: Google It | Yahoo | Bing
Cruise Ship Reviews | Luxury Resort | Jet | Yacht | and Travel Tech More Info
Cruising Review Topics and Articles More Info
Software based on Filemaker for the travel industry More Info
The Burgenstock Resort: Reviews on CruisingReview website... More Info
Resort Reviews: World Class resorts... More Info
The Riffelalp Resort: Reviews on CruisingReview website... More Info
CONTACT TEL: 608-238-6001 Email: greg@cruisingreview.com (Standard Web Page)