Background: Pterygium is a sun-related ocular surface disease secondary to ultraviolet (UV) radiation exposure. Outdoor occupational UV exposure is known to occur secondary to sun exposure. We present a unique case of pterygium associated with indoor occupational light-emitting diode (LED) exposure not previously described in the literature.
Case Description: A mobile phone repairer presented with blurred vision and a superotemporal pterygium of his dominant left eye associated with a magnifying glass LED work lamp was diagnosed. This was excised routinely with conjunctival autografting to the defect. Histopathology confirmed benign pterygium and recovery was uncomplicated with resolution of blur.
Conclusions: The development of pterygium in our patient may have arisen due to the LED lamp’s wavelengths possibly falling within the UV as well as the upper end of the visible light radiation spectrum. Given the increasing reliance on LED light sources in modern life, ocular conditions arising from exposure to these radiation sources may now need to be listed in the differential diagnoses of patients with pterygium. Appropriate UV protection counselling for these types of lights may also now need to be considered.
Abstract: Blinding diseases such as photoreceptor degenerations are debilitating conditions that severely impair daily lives of affected patients. This group of diseases are amenable to photoreceptor replacement therapies and recent transplantation studies provided proof-of-principle for functional recovery at the retinal and behavioral level, though the actual mechanism of repair still needs further investigations. The immune system responds in several ways upon photoreceptor engraftment, resulting in T-cell and macrophage infiltrations and, consequently, decrease in graft survival. Most studies on the role of the immune system suggest a detrimental effect in a therapeutic setting. Conversely, the opposite idea wherein the immune system can be activated towards a protective state was also explored in other experimental paradigms. Here, Neves and colleagues explored the potential of cross-species studies and, to a certain extent, the concept of a protective immune system in retinal degeneration and therapy. Mesencephalic astrocyte-derived neurotrophic factor (MANF) was identified in this study as a novel factor that, by modulating the immune system, can slow down photoreceptor degeneration and improve transplantation outcome.
Background: The usage of the light emitting diode (LED) has been increasingly applied in the illumination setting and electronic equipment. However, the effect of LED lights on the retina remains unclear. In this study, we observed and analyzed the impact of white LED lights at different intensities on the function and morphology of rat retinas.
Methods: Thirty-six Sprague-Dawley rats weighing 150–180 g were randomly divided into six groups (n=6 in each group) including a normal control (NC) group, 4 white LED groups at different light intensities (4,000, 6,000, 7,000, and 10,000 lux), and an ultraviolet B (UVB) lighting group (302 nm, 1,000 μw/cm2). After 24 hours of continuous illumination, full-field flash electroretinogram (FERG) and pathological examination were performed in each group.
Results: As revealed by FERG, the impairment of retinal function gradually worsened with the increase of LED light intensity. In contrast, the UVB group had the most severe retinal function impairment. Particularly, the functional damage of rod cells and inner nuclear layer cells was the main FERG finding in each group. In the NC group, the retina had typical morphologies featured by well-defined structures, clearly visible border between the inner and outer segments, and neatly arranged inner and outer nuclear layer cells. After 24 hours of illumination, the inner and outer parts of the retina in the 4,000 lux group were still neatly arranged, along with a clear border; however, the inner and outer nuclear layers were randomly arranged, and some irregular nuclei and cells were lost. The damage of the internal and external retinal segments and the internal and external nuclear layers became more evident in the 6,000 lux group, 7,000 lux group, and 10,000 lux group. The UVB group had a more obviously disordered arrangement of inner and outer nuclear layers and loss of cells.
Conclusions: Continuous exposure to white LED light can cause structural and functional damage to rat retinas, and such damage is related to the intensity of illumination. Therefore, the risk of retinal damage should be considered during LED illumination, and proper LED illumination intensity may help to maintain eye health.
Objective: In this review, non-transgenic models of age-related macular degeneration (AMD) are discussed, with focuses on murine retinal degeneration induced by sodium iodate and lipid peroxide (HpODE) as preclinical study platforms.
Background: AMD is the most common cause of vision loss in a world with an increasingly aging population. The major phenotypes of early and intermediate AMD are increased drusen and autofluorescence, Müller glia activation, infiltrated subretinal microglia and inward moving retinal pigment epithelium (RPE) cells. Intermediate AMD may progress to advanced AMD, characterized by geography atrophy and/or choroidal neovascularization (CNV). Various transgenic and non-transgenic animal models related to retinal degeneration have been generated to investigate AMD pathogenesis and pathobiology, and have been widely used as potential therapeutic evaluation platforms.
Methods: Two retinal degeneration murine models induced by sodium iodate and HpODE are described. Distinct pathological features and procedures of these two models are compared. In addition, practical protocol and material preparation and assessment methods are elaborated.
Conclusions: Retina degeneration induced by sodium iodate and HpODE in mouse eye resembles many clinical aspects of human AMD and complimentary to the existent other animal models. However, standardization of procedure and assessment protocols is needed for preclinical studies. Further studies of HpODE on different routes, doses and species will be valuable for the future extensive use. Despite many merits of murine studies, differences between murine and human should be always considered.
Background: Retinal degeneration is a common feature of several retinal diseases, such as retinitis pigmentosa and age-related macular degeneration (AMD). In this respect, experimental models of photo-oxidative damage reproduce faithfully photoreceptor loss and many pathophysiological events involved in the activation of retinal cell degeneration. Therefore, such models represent a useful tool to study the mechanisms related to cell death. Their advantage consists in the possibility of modulating the severity of damage according to the needs of the experimenter. Indeed, bright light exposure could be regulated in both time and intensity to trigger a burst of apoptosis in photoreceptors, allowing the study of degenerative mechanisms in a controlled fashion, compared to the progressive and slower rate of death in other genetic models of photoreceptor degeneration.
Methods: Here, an exemplificative protocol of bright light exposure in albino rat is described, as well as the main outcomes in retinal function, photoreceptor death, oxidative stress, and inflammation, which characterize this model and reproduce the main features of retinal degeneration diseases.
Discussion: Models of photo-oxidative damage represent a useful tool to study the mechanisms responsible for photoreceptor degeneration. In this respect, it is important to adapt the exposure paradigm to the experimental needs, and the wide range of variables and limitations influencing the final outcomes should be considered to achieve proper results.
Trial Registration: None.
