Solar Retinopathy

Jain, Atul; Desai, Rajen U.; Charalel, Resmi A.; Quiram, Polly A.; Yannuzzi, Lawrence A.; Sarraf, David

doi:10.1097/iae.0b013e3181b0da88

Cited by 52 publications

(33 citation statements)

References 14 publications

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“… 135 A retrospective observational study demonstrated defects in photoreceptor ISel bands with foveal atrophy in all patients on SD-OCT, whereas FA identified classic window defects in only a few eyes. 136 In addition to distinct defects in the photoreceptor ISel band and photoreceptor outer segments, bilateral foveal thinning was demonstrated on high-speed ultra high definition OCT in a 34-year-old man with chronic solar retinopathy. 137 An observational case series demonstrated abnormally high reflectivity in the outer foveal retina as disruption of the photoreceptor ISel band and full thickness involvement of the photoreceptor layer was associated with poor visual acuity.…”

Section: Inner Segment Ellipsoid In Medical Retinal Diseasesmentioning

confidence: 92%

Photoreceptor inner segment ellipsoid band integrity on spectral domain optical coherence tomography

Saxena¹,

Srivastav²,

Cheung³

et al. 2014

OPTH

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Spectral domain optical coherence tomography cross-sectional imaging of the macula has conventionally been resolved into four bands. However, some doubts were raised regarding authentication of the existence of these bands. Recently, a number of studies have suggested that the second band appeared to originate from the inner segment ellipsoids of the foveal cone photoreceptors, and therefore the previously called inner segment-outer segment junction is now referred to as inner segment ellipsoidband. Photoreceptor dysfunction may be a significant predictor of visual acuity in a spectrum of surgical and medical retinal diseases. This review aims to provide an overview and summarizes the role of the photoreceptor inner segment ellipsoid band in the management and prognostication of various vitreoretinal diseases.

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Section: Inner Segment Ellipsoid In Medical Retinal Diseasesmentioning

confidence: 92%

Photoreceptor inner segment ellipsoid band integrity on spectral domain optical coherence tomography

Saxena¹,

Srivastav²,

Cheung³

et al. 2014

OPTH

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“…Light-induced retinal damage can be a problem after acute or chronic sun exposure and surgery (Fuller et al, 1978; Zigman et al, 1979; Kuhn et al, 1991; Thanos et al, 2001; Codenotti et al, 2002; Jain et al, 2009; Vojnikovic et al, 2009). Excessive light may accelerate the loss of vision and serves as a physiologic model for human retinal degenerative diseases such as age-related macular degeneration (AMD) (Marc et al, 2008; Organisciak and Vaughan, 2010).…”

Section: Introductionmentioning

confidence: 99%

NAD+ maintenance attenuates light induced photoreceptor degeneration

Bai

Sheline

2013

Experimental Eye Research

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Light-induced retinal damage (LD) occurs after surgery or sun exposure. We previously showed that zinc (Zn2+) accumulated in photoreceptors and RPE cells after LD but prior to cell death, and pyruvate or nicotinamide attenuated the resultant death perhaps by restoring nicotinamide adenine dinucleotide (NAD+) levels. We first examined the levels of NAD+ and the efficacy of pyruvate or nicotinamide in oxidative toxicities using primary retinal cultures. We next manipulated NAD+ levels in vivo and tested the affect on LD to photoreceptors and RPE. NAD+ levels cycle with a 24-h rhythm in mammals, which is affected by the feeding schedule. Therefore, we tested the affect of increasing NAD+ levels on LD by giving nicotinamide, inverting the feeding schedule, or using transgenic mice which overexpress cytoplasmic nicotinamide mononucleotide adenyl-transferase-1 (cytNMNAT1), an NAD+ synthetic enzyme. Zn2+ accumulation was also assessed in culture and in retinal sections. Retinas of light damaged animals were examined by OCT and plastic sectioning, and retinal NAD levels were measured. Day fed, or nicotinamide treated rats showed less NAD+ loss, and LD compared to night fed rats or untreated rats without changing the Zn2+ staining pattern. CytNMNAT1 showed less Zn2+ staining, NAD+ loss, and cell death after LD. In conclusion, intense light, Zn2+ and oxidative toxicities caused an increase in Zn2+, NAD+ loss, and cell death which were attenuated by NAD+ restoration. Therefore, NAD+ levels play a protective role in LD-induced death of photoreceptors and RPE cells.

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“…Light-induced retinal damage can occur after acute or chronic sun exposure and surgery (Fuller et al, 1978; Zigman et al, 1979; Kuhn et al, 1991; Thanos et al, 2001; Codenotti et al, 2002; Jain et al, 2009; Vojnikovic et al, 2009). Light also accelerates disease progression and neurodegeneration in many retinal diseases in which light or oxidative stress (OS) are implicated (RP, glaucoma, macular degeneration) (Wang et al, 1997; Bicknell et al, 2002; Organisciak et al, 2003; Ranchon et al, 2003; Richards et al, 2006; Vaughan et al, 2006; Yang et al, 2007; Rodriguez and Fliesler, 2009) (Reviewed in (Organisciak and Vaughan, 2010)).…”

Section: Introductionmentioning

confidence: 99%

A reduced zinc diet or zinc transporter 3 knockout attenuate light induced zinc accumulation and retinal degeneration

Bai

Sheline

Zhou

et al. 2013

Experimental Eye Research

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Our previous study on retinal light exposure suggests the involvement of zinc (Zn2+) toxicity in the death of RPE and photoreceptors (LD) which could be attenuated by pyruvate and nicotinamide, perhaps through restoration of NAD+ levels. In the present study, we examined Zn2+ toxicity, and the effects of NAD+ restoration in primary retinal cultures. We then reduced Zn2+ levels in rodents by reducing Zn2+ levels in the diet, or by genetics and measured LD. Sprague Dawley albino rats were fed 2, or 61 mg Zn2+/kg of diet for 3 weeks, and exposed to 18 kLux of white light for 4h. We light exposed (70 kLux of white light for 50h) Zn2+ transporter 3 knockout (ZnT3-KO, no synaptic Zn2+), or RPE65 knockout mice (RPE65-KO, lack rhodopsin cycling), or C57/BI6/J controls and determined light damage and Zn2+ staining. Retinal Zn2+ staining was examined at 1h and 4h after light exposure. Retinas were examined after 7d by optical coherence tomography and histology. After LD, rats fed the reduced Zn2+ diet showed less photoreceptor Zn2+ staining and degeneration compared to a normal Zn2+ diet. Similarly, ZnT3-KO and RPE65-KO mice showed less Zn2+ staining, NAD+ loss, and RPE or photoreceptor death than C57/BI6/J control mice. Dietary or ZnT3-dependent Zn2+ stores, and intracellular Zn2+ release from rhodopsin recycling are suggested to be involved in light-induced retinal degeneration. These results implicate novel rhodopsin-mediated mechanisms and therapeutic targets for LD. Our companion manuscript demonstrates that pharmacologic, circadian, or genetic manipulations which maintain NAD+ levels reduce LD.

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Solar Retinopathy

Cited by 52 publications

References 14 publications

Photoreceptor inner segment ellipsoid band integrity on spectral domain optical coherence tomography

Photoreceptor inner segment ellipsoid band integrity on spectral domain optical coherence tomography

NAD+ maintenance attenuates light induced photoreceptor degeneration

A reduced zinc diet or zinc transporter 3 knockout attenuate light induced zinc accumulation and retinal degeneration

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