Blue Light Damage Research Articles

Cs2MnCl4:Eu2+: A Near-Violet Light-Triggered Single-Component White Light Emitter.

Single-component white-light luminescent materials are considered an economical and facile choice for phosphor-converted white light-emitting diodes (pc-WLEDs). Here, a new single-component white-light-emitting material Cs2MnCl4:Eu2+ based on the combination of a lead-free halide structure and a rare-earth ion is first reported. Benefiting from the smart dilution-sensitization design strategy, white light composed of dual broad emission originating from Eu2+ (blue light, 444 nm, 4f65d1 → 4f7) and Mn2+ (yellow light, 566 nm, 4T1g → 6A1g) was successfully realized under near-ultraviolet light (404 nm) radiation with a high photoluminescence quantum yield of 66%. Based on the single-source Cs2MnCl4:Eu2+ phosphor, a pc-WLEDs device with "eye-friendly" white light production was successfully fabricated. The pc-WLEDs exhibit suitable color coordinates of (0.3294, 0.2746) and a high color rendering index of 82.3, demonstrating the potential in the future health-conscious illumination application by reducing the risk of eye strain and high-energy blue-light damage. This work achieves a new single-component white-light-emitting Mn-based halide phosphor and provides a new path for the design of single-component white light sources in Mn-based halides.

Differences between long- and short-wavelength light–induced retinal damage and the role of PARP-1 in retinal injury induced by blue light

Photobiomodulation (PBM) therapy uses light of different wavelengths to treat various retinal degeneration diseases, but the potential damage to the retina caused by long-term light irradiation is still unclear. This study were designed to detect the difference between long- and short-wavelength light (650-nm red light and 450-nm blue light, 2.55 mW/cm2, reference intensity in PBM)–induced injury. In addition, a comparative study was conducted to investigate the differences in retinal light damage induced by different irradiation protocols (short periods of repeated irradiation and a long period of constant irradiation). Furthermore, the protective role of PARP-1 inhibition on the molecular mechanism of blue light-induced injury was confirmed by a gene knockdown technique or a specific inhibitor through in vitro and in vivo experiments. The results showed that the susceptibility to retinal damage caused by irradiation with long- and short-wavelength light is different. Shorter wavelength lights, such as blue light, induce more severe retinal damage, while the retina exhibits better resistance to longer wavelength lights, such as red light. In addition, repeated irradiation for short periods induces less retinal damage than constant exposure over a long period. PARP-1 plays a critical role in the molecular mechanism of blue light-induced damage in photoreceptors and retina, and inhibiting PARP-1 can significantly protect the retina against blue light damage. This study lays an experimental foundation for assessing the safety of phototherapy products and for developing target drugs to protect the retina from light damage.

Green‐Emissive Carbon Dots with a High Quantum Yield Applied for Photoconversion Film to Prevent from Blue Light Damage

AbstractHigh‐energy blue light is highly detrimental to health as it can penetrate the lens into the retina, potentially causing atrophy or even death of retinal pigment epithelial cells. To prevent the harmful effects of high‐energy blue light on our health, here the preparation of a photoconversion film specifically designed to block high‐energy blue light is reported, which is composed of green‐emissive carbon dots (G‐CDs) with a high photoluminescence quantum yield (PLQY = 95%) dispersed in polyvinyl alcohol (PVA) matrix. Notably, such a film (named as G‐CDs@PVA) not only converts an incident laser light with a short wavelength into a fluorescence with a longer wavelength, but also exhibits concentration‐dependent (0, 10, 20, and 30 wt.%) blue light barrier rate and green‐emissive intensity. With the increase of the concentration of G‐CDs in the film, the blue light barrier rate of the film as well as the maximum intensity of the green emission are also increased. When the concentration of G‐CDs reaches 30 wt.%, the blue light barrier rate of G‐CDs@PVA achieves up to 97%. Furthermore, G‐CDs@PVA film is attached to a blue light‐emitting diode (LED) chip to explore its practical application in the field of blocking blue light damage.

Relative bioavailability of lutein and zeaxanthin in the presence of Omega-3- supplements and oxidative stress levels in humans

Lutein and zeaxanthin (LZ) are the major constituents of macular pigment (MP), helping to protect the human retina from blue light and oxidative damage(1). Many studies have suggested that higher concentrations of retina LZ may reduce the risk of age-related macular degeneration (AMD) and improve retinal health(1–3). MP and serum L have shown positive linear response with L dose(4) but the combined effect (LZ + omega-3 suppl) has not been fully explored in healthy Australian adults. Understanding their bioavailability in relation to the effect of omega-3 fatty acid intakes along with LZ supplements could provide a useful indication of the potential to reduce the risk of AMD, preserve vision, and improve retinal health. LZ uptake and the associated oxidative stress levels were evaluated in two groups fed with commercially sourced supplements. The control group was given only LZ, while the intervention group was given LZ combined with omega-3 supplements containing Eicosapentaenoic acid (EPA) and Docosahexaenoic acid (DHA). 10 men and 6 women with an average age of 31.4 ± 1.3yrs participated in this randomised, non-blinded controlled study for a total of 19-d. The control group (9) consumed the LZ supplement (12mg/d) only, while the intervention group (7) consumed the LZ supplement along with 900mg/d of an omega-3 supplement (540mg EPA + DHA 360mg). Each group adhered to a comprehensive low-carotenoid and omega-3 diet list for the 12-d intervention period and the 7-d washout period. Participants reported daily foods consumed in their diet logbooks, and Automated Self-Administered 24 diet assessment log over the study period. The body composition of each subject from the two groups was assessed before and after the study using a SECA body composition analyser and blood samples (2-time point) collected over a 12-d test period. Mean ± SEM for serum LZ ranged from 2.23 ± 0.24 – 2.98 ± 0.24µg/ml for the control group and 1.10 ± 0.21–3.02 ± 0.73µg/ml for the intervention group. Percentage change in serum LZ concentration from (T0-T312h) and (T312h-T456h) were 26% and 34% (control) and 139% and 175% for (intervention), respectively. The Area Under the Curve (AUC0-456h) differed significantly (P<0.0469) during the entire study period (between groups) and related to the cumulative effect of intakes at various times of blood draw. LZ from the intervention group was 68% more bioavailable than the control group. The highest peak relative response in subjects in the control group was ≈33% (a 9.1-fold increase from baseline) at AUC (168-312h) and ≈46% (a 6.6-fold increase from baseline) at AUC (312-456h) for the intervention group. No significant (p>0.05) effect of omega-3-supplement addition on oxidative stress levels was observed. Omega-3- addition to intakes of supplement LZ was responsible for the increased absorption (intervention) observed but did not affect oxidative stress levels and the Red Blood Cell omega-3-status.

Blue Light Damage and p53: Unravelling the Role of p53 in Oxidative-Stress-Induced Retinal Apoptosis.

In the digital age, the widespread presence of electronic devices has exposed humans to an exceptional amount of blue light (BL) emitted from screens, LEDs, and other sources. Studies have shown that prolonged exposure to BL could have harmful effects on the visual system and circadian rhythm regulation. BL is known to induce oxidative stress, leading to DNA damage. Emerging research indicates that BL may also induce cell death pathways that involve the tumor-suppressor protein p53. Activated p53 acts as a transcription factor to regulate the expression of genes involved in cell cycle arrest, DNA repair, and apoptosis. This study aimed to explore the implication of p53 in BL-caused retinal damage, shedding light on the potential mechanisms of oxidative-stress-induced retinal diseases. BL-exposed porcine retinal cultures demonstrated increased p53- and caspase-mediated apoptosis, depending on exposure duration. Direct inhibition of p53 via pifithrin α resulted in the prevention of retinal cell death. These findings raise concerns about the long-term consequences of the current daily BL exposure and its potential involvement in various pathological conditions, including oxidative-stress-based retinal diseases like age-related macular degeneration. In addition, this study paves the way for the development of novel therapeutic approaches for oxidative-stress-based retinal diseases.

Active Components of Leontopodium alpinum Callus Culture Extract for Blue Light Damage in Human Foreskin Fibroblasts.

Leontopodium alpinum is a source of raw material for food additives and skin health. The purpose of this study was to investigate the application of Leontopodium alpinum callus culture extract (LACCE) to prevent blue light damage to the skin. We screened and identified the blue light-damage-protecting activities and mechanisms of ten components of LACCE, including chlorogenic acid (A), isoquercitrin (B), isochlorogenic acid A (C), cynaroside (D), syringin (E), isochlorogenic acid (F), cynarin (G), rutin (H), leontopodic acid A (I), and leontopodic acid B (J), using a novel blue light-induced human foreskin fibroblast (HFF-1) cell injury model. The study examined the cytotoxicity of ten ingredients using the cell counting kit-8 (CCK-8) assay, and selecting concentrations of 5, 10, and 20 μM for experiments with a cell viability above 65%. We explored the effects and mechanisms of action of these LACCE components in response to blue light injury using Western blotting and an enzyme-linked immunosorbent assay. We also measured ROS secretion and Ca2+ influx. Our study revealed that leontopodic acid A effectively boosted COI-1 expression, hindered MMP-1 expression, curbed ROS and Ca2+ endocytosis, and reduced OPN3 expression. These results provide theoretical support for the development of new raw materials for the pharmaceutical and skincare industries.

Rutin intake mitigates the injury of blue light irradiation by altering aging rates of mortality in Drosophila model.

Blue light is known as one of the harmful light pollution that has complex effects on organisms. The massive use of LED lights in cities has greatly increased the frequency of human exposure to blue light, and therefore the hazards of blue light are receiving widespread attention. In our study, Drosophila was used as the model organism to explore the ability of the flavonoid rutin to resist blue light damage under the intensity of 3000 Lux. Siler model analysis was performed. Our results showed sex-specific pattern of rutin as an effective antioxidant. Rutin could help female flies to reduce the initial adult mortality and male flies to slow the increase of adult mortality under blue light irradiation, thus prolonging their average lifespan. Furthermore, after the intake of rutin, the locomotor activity of Drosophila under blue light irradiation was significantly increased, and the total sleep time was significantly decreased. In summary, our results provide preliminary support for exploring the mechanism of rutin against blue light damage.

REG1A protects retinal photoreceptors from blue light damage.

With the increased use of artificial light and the prolonged use of optoelectronic products, light damage (LD) to the human retina has been identified as a global vision-threatening problem. While there is evidence of a significant correlation between light-induced retinal damage and age-related vision impairment in age-related macular degeneration, it is unclear how light-induced retinal degeneration manifests itself and whether there are agents capable of preventing the development of LD in the retina. This study investigated a mechanism by which blue light leads to photoreceptor death. By observing blue light exposure in retinal organoids and photoreceptor cells, we concluded that there could be significant apoptosis of the photoreceptors. We demonstrate that regenerating islet-derived 1 alpha (REG1A) prevents photoreceptors from undergoing this LD-induced apoptosis by increasing expression of the anti-apoptotic gene Bcl2 and downregulating expression of the pro-apoptotic gene Bax, resulting in reduced mitochondrial damage and improved aerobic capacity in photoreceptor cells. For the first time, REG1A has been shown to restore mitochondrial function and cell apoptosis after LD-induced damage, suggesting its potential application in the prevention and treatment of retinal vision loss.

Blue Light and Eye Damage: A Review on the Impact of Digital Device Emissions

The pandemic and lockdown caused by COVID-19 accelerated digitalization. Personal digital devices, emitting high-energy light, namely in the blue wavelength, have raised concerns about possible harmful effects on users’ eyes. Scientific research history has shown a relationship between exposure to blue light and changes in ocular structures. The main goal of this review is to examine frequent and prolonged exposure to blue radiation from computers, tablets and smartphones and its consequences on vision and ocular structures. Bibliographic research was carried out on changes induced by blue light in ocular structures, the cornea, the crystalline lens and the retina based on the following scientific databases: BioOne Complete™; Google Scholar™; Paperity™; PubMed™; and ScienceOpen™. The most significant studies on blue light and ocular damage were selected and reviewed. The most relevant bibliographic data were analyzed and summarized and some gaps in the theme of blue light from digital devices were identified. The experimental need to acquire additional new data is suggested. The hypothesis that continued use of digital devices enriched with blue light may interfere with the biological tissues of the cornea, crystalline lens, or retina is not clarified in the available scientific evidence. Therefore, additional studies are needed to answer this problem.

Effects and Mechanism of the Leontopodium alpinum Callus Culture Extract on Blue Light Damage in Human Foreskin Fibroblasts

Leontopodium alpinum is an important source of raw material for food, medicine, and modern cosmetics. The purpose of this study was to develop a new application for protection against blue light damage. To investigate the effects and mechanism of action of Leontopodium alpinum callus culture extract (LACCE) on blue light damage, a blue-light-induced human foreskin fibroblast damage model was established. The contents of collagen (COL-I), matrix metalloproteinase 1 (MMP-1), and opsin 3 (OPN3) were detected using enzyme-linked immunosorbent assays and Western blotting. The calcium influx and reactive oxygen species (ROS) levels were measured via flow cytometry and the results showed that the LACCE (10-15 mg/mL) promoted the production of COL-I, inhibited the secretion of MMP-1, OPN3, ROS and calcium influx, and may play a role in inhibiting the activation of blue light on the OPN3-calcium pathway. Thereafter, high-performance liquid chromatography and ultra-performance liquid chromatography-tandem mass spectrometry were used to quantitatively analyze the contents of nine active ingredients in the LACCE. The results indicated that LACCE has an anti-blue-light-damage effect and provides theoretical support for the development of new raw materials in the natural food, medicine, and skin care industries.

Reproducible method for assessing the effects of blue light using in vitro human skin tissues.

High-intensity visible light (HEV), also referred to as blue light, has a wavelength of 400-500 nm and accounts for approximately one-third of the visible light. Blue light is also emitted from electronic devices and artificial indoor lighting. Studies have shown that exposure of human skin cells to light emitted from electronic devices, even as short as 1 h, can cause an increase in reactive oxygen species (ROS), apoptosis and necrosis. Despite comprising a significant portion of the light spectrum, the effects of HEV light have not been studied as extensively. This is in part due to a lack of suitable in vitro testing methods. This work was conducted in order to develop a reproducible testing method for assessing the effects of blue light on the skin. Testing was performed using a full thickness, 3D in vitro skin tissue model. Different exposure protocols were tested to (1) determine the biological effects of blue light on the skin and (2) to identify an appropriate exposure for routine testing of cosmetic materials that may protect the skin from blue light damage. Gene expression and protein biomarkers were measured using qPCR, ELISA and immunohistochemical (IHC) methods. Our work demonstrates that daily exposure to blue light produced dose-and-time-dependent changes in biomarkers associated with skin damage. Exposure to blue light for 6 h for 5 consecutive days (total intensity of 30 J/cm2 ) increased the expression of genes that regulate inflammation and oxidative stress pathways and decreased the expression of genes that maintain skin barrier and tissue integrity. Exposure to blue light significantly increased protein biomarkers associated with ageing, inflammation and tissue damage. IHC staining confirmed changes in collagen, filaggrin and NQO1 protein expression. Treatment with ascorbic acid inhibited the effects of blue light, demonstrating a role in protection from blue light. Our results showed that consistent blue light exposure produced skin damage via alterations in biological pathways that are associated with skin ageing. This work provides a new, reproducible in vitro testing method for assessing the effects of blue light on human skin using gene expression, protein ELISA and IHC staining.

Retinal protective effect of curcumin metabolite hexahydrocurcumin against blue light-induced RPE damage

BackgroundAge-related macular degeneration (AMD) is a disease of retinal pigment epithelium (RPE) cells. We have previously demonstrated that blue light can damage RPE cells and their underlying mechanisms. We found that hexahydrocurcumin (HHC), a metabolite of curcumin, had better retinal protection than curcumin. However, the involved mechanisms remain unclear. MethodsBy exposing ARPE-19 human RPE cells and mouse primary RPE cells to blue light, the intracellular mechanisms of HHC in cells were investigated, including the proliferation of RPE cells and the effects of HHC on activating intracellular protective mechanisms and related factors. Next-generation sequencing (NGS) RNA sequencing revealed the underlying mechanisms involved in the induction and regulation of HHC treatment following blue light exposure. ResultsHHC promoted autophagy by enhancing autophagic flux, reduced oxidative stress and endoplasmic reticulum (ER) stress, and effectively reversed blue light-induced cell death. RNA sequencing-based bioinformatics approaches comprehensively analyze HHC-mediated cellular processes. ConclusionOur findings elucidate the mechanisms of HHC against blue light damage in RPE cells and are beneficial for the development of natural metabolite-based preventive drugs or functional foods.

In vitro and in vivo characterization of BIO203, a new amide norbixin conjugate with improved pharmacokinetic profile. Potential for oral treatment of age‐related retinal degeneration

AbstractPurpose: We have previously shown that 9′‐cis‐norbixin (norbixin) protects retinal pigmented epithelium (RPE) cells against phototoxicity induced by blue light and N‐retinylidene‐N‐retinylethanolamine (A2E) in vitro and preserves visual function in animal models of dry Age‐related Macular Degeneration (AMD) in vivo. The purpose of this study was to examine the mode of action and the in vitro and in vivo effects of CN30, a norbixin monoamide conjugate.Methods: Ocular pharmacokinetics in rats administered orally with 50 mg/kg of norbixin, or its conjugate (CN30) were compared. Their effect on photoprotection of primary porcine RPE cells challenged with A2E and blue‐light illumination was quantified. The effects of CN30 on the A2E‐induced transactivation of PPARs, AP‐1 and NF‐κB were measured by reporter gene luciferase activity. The expression of IL‐6, IL‐8, and VEGF was measured by RT‐QPCR. The in vivo neuroprotective effect of intraperitoneally administered CN30 was evaluated by measuring retinal thickness and electroretinogram (ERG) amplitudes in a blue‐light damage (BLD) acute model in albino rats. CN30 efficacy was also assessed by ERG after 6 months oral supplementation in Abca4−/− Rdh8−/− mice.Results: Compared to norbixin, CN30 displays improved stability and enhanced ocular maximal concentration and exposure (AUC). Similar to our previous observation with norbixin, CN30 mode of action involves the inhibition of PPARs, NF‐κB and AP‐1 transactivation. CN30 reduces IL‐6, IL‐8 and VEGF expression induced by A2E in vitro. In vivo, CN30 protects visual function and retinal structure in albino rats subjected to BLD in an acute model of retinal degeneration. Moreover, 6 months oral supplementation also improve visual function in a model of dry AMD: the Abca4−/− Rdh8−/− double knock‐out mice.Conclusions: CN30 retains the protective properties of norbixin in vitro and in vivo, and displays improved stability and pharmacokinetic properties. This could open new avenues for the oral treatment of retinal degenerative diseases such as dry AMD.

A dual-emission Ba6Ca3Al2Si6O24: Eu2+, Mn2+ phosphor with energy transfer for plant-protecting LED lamps and ratiometric temperature

A series of dual-emitting Eu2+-Mn2+ co-doped Ba6Ca3Al2Si6O24 (BCASO) phosphors were prepared by a solid phase method at high temperature. The phosphors show a blue-green emission peaking at 500 nm and a red emission peaking at 600 nm under a single UV excitation, which facilitates the absorption of Chlorophyll a/b and Phytochrome PR, while avoiding excessive blue light damage to plants and energy wastage. The reason for the simultaneous appearance of blue-green and red light is the energy transfer from Eu2+ to Mn2+. The corresponding process has been investigated by analyzing the spectrum and the decay lifetime variations. In addition, we have explored the thermal stability of the phosphors, which is also an important parameter especially in plant lighting. We have unexpectedly found that Eu2+ and Mn2+ ions have different thermal reactions during the stability study, which has opened up the possibility for temperature detection. Therefore, we have discussed temperature measurement characteristics, such as the relationship between FIR and T, absolute sensitivity (Sa) and relative sensitivity (Sr). The results confirmed that the BCASO: Eu2+, Mn2+ phosphor might have great applicational potential in plant-protecting and optical temperature measurement.

28.1: Invited Paper: The Application of Wide Spectrum Low Peak Blue light technology in health TV display

This paper reports a method to reduce the high energy and short wave blue light damage to human eyes, by reducing the proportion of blue light in using two chips in LED as blue light chips with different main wavelengths. At the same time, the filter blue light particle are coated on the membrane to remove high‐energy short wave blue light to achieve eye protection effect. The project can increase the half‐wave width to 25 nm and reduce the blue light peak to 50%, so that the wide spectrum of the display screen is close to the continuous spectrum of natural light. The above scheme will not affect the brightness and gamut. Meanwhile, that project can maintain the original color temperature of the display, provide the best viewing effect and safeguard the human eye health while protecting the health of the users.

Assessment of Antioxidant Potential of Lutein, a Retinol Equivalent Carotenoid in Medicinal Landrace of Rice ‘Kavuni’

Background: Indigenous traditional coloured rices are rich in dietary fibre, resistant starch, minerals, bioactive compounds and antioxidants like anthocyanins, luteins and phenols. Kavuni is one such brownish black medical landrace of rice considered as nutrition supplement since 400BC as it cures gastritis, peptic ulcer and also enhances blood circulation and known for its anti diabetic and anti-inflammatory properties. Lutein is the only dietary oxycarotenoid found in both the macula and lens of the human eye, and acts as blocker of blue light damage, quench reactive oxygen species, prevent age related macular degeneration, cataracts, cardiovascular disease and lung cancer.
 Aim: The objective of the present investigation was to characterize the lutein content and antioxidant potential of Kavuni and released mega varieties of rice (ASD 16, Swarna Sub1) and its derivatives obtained from crosses ASD 16 and Kavuni; Swarna Sub1 and Kavuni.
 Methodology & Results: It was found that lutein (quantified by HPLC) was much higher in Kavuni (225 µg/100 g) compared with white rice varieties (ASD 16-15 µg/100g and Swarna Sub1-21 µg/100 g) and the DPPH (2, 2-diphenyl-1-picrylhydrazyl) scavenging ability (for quantification of antioxidant potential) were in the order (Kavuni >>ASD16, Swarna Sub1. Pigmented grain genotypes having higher lutein content had higher percentage of free radical scavenging activity of DPPH and lower IC50 values compared to non pigmented genotypes.
 Conclusion: It is conceivable that the medicinal landraces of rice could be exploited as one of the potential sources for plant - based pharmaceutical products.

Whole transcriptome analysis on blue light-induced eye damage.

To analyze abnormal gene expressions of mice eyes exposed to blue light using RNA-seq and analyze the related signaling pathways. Kunming mice were divided into an experimental group that was exposed to blue light and a control group that was exposed to natural light. After 14d, the mice were euthanized and their eyeballs were collected. Whole transcriptome analysis was attempted to analyze the gene expression of the eyeballs using RNA-seq to reconstruct genetic networks. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to reveal the related signaling pathways. The 737 differentially expressed genes were identified, including 430 up and 307 down regulated genes, by calculating the gene FPKM in each sample and conducting differential gene analysis. GO and KEGG pathway enrichment analysis showed that blue light damage may associated with the visual perception, sensory perception of light stimulus, phototransduction, and JAK-STAT signaling pathways. Differential lncRNA, circRNA and miRNA analysis showed that blue light exposure affected pathways for retinal cone cell development and phototransduction, among others. Exposure to blue light can cause a certain degree of abnormal gene expression and modulate signaling pathways in the eye.

Systemic administration of the di-apocarotenoid norbixin (BIO201) is neuroprotective, preserves photoreceptor function and inhibits A2E and lipofuscin accumulation in animal models of age-related macular degeneration and Stargardt disease.

Atrophic A\\age-related macular degeneration (AMD) and Stargardt disease (STGD) are major blinding diseases affecting millions of patients worldwide, but no treatment is available. In dry AMD and STGD oxidative stress and subretinal accumulation of N-retinylidene-N-retinylethanolamine (A2E), a toxic by-product of the visual cycle, causes retinal pigment epithelium (RPE) and photoreceptor degeneration leading to visual impairment. Acute and chronic retinal degeneration following blue light damage (BLD) in BALB/c mice and aging of Abca4-/- Rdh8-/- mice, respectively, reproduce features of AMD and STGD. Efficacy of systemic administrations of 9'-cis-norbixin (norbixin), a natural di-apocarotenoid, prepared from Bixa orellana seeds with anti-oxidative properties, was evaluated during BLD in BALB/c mice, and in Abca4-/- Rdh8-/- mice of different ages, following three experimental designs: “preventive”, “early curative” and “late curative” supplementations. Norbixin injected intraperitoneally in BALB/c mice, maintained scotopic and photopic electroretinogram amplitude and was neuroprotective. Norbixin chronic oral administration for 6 months in Abca4-/- Rdh8-/- mice following the “early curative” supplementation showed optimal neuroprotection and maintenance of photoreceptor function and reduced ocular A2E accumulation. Thus, norbixin appears promising as a systemic drug candidate for both AMD and STGD treatment.

Blaulichtgefährdung der Augen durch Lichtemittierende Dioden (LED)?

Blue light from light-emitting diodes (LED): a risk to the eyes? Background: In occupational and domestic environments people are increasingly exposed to artificial light from light-emitting diodes (LEDs). LEDs have peak emission in the blue range. In this review, we summarise the current knowledge of the possible effects of blue light exposure on ocular health. Effects of blue light on the regulation of physiological functions will be considered elsewhere. Methods: We performed a narrative review. We included preclinical data as well as epidemiological studies. We searched MEDLINE, Pubmed, the Cochrane Library and International Standard Randomised Controlled Trial Number (ISRCTN)-Register clinical trial registers from 01 January 2014 to 31 May 2019. Results: The accumulated experimental evidence obtained from different experimental models has indicated that excessive exposure to blue light can induce damage in the retinal pigment epithelium (RPE), in photoreceptors and ganglion cells. Previous epidemiological findings are equivocal regarding any causal links between blue light exposure and the development of macular degeneration (AMD). In vitro and in vivo evidence suggests that blue light exposure may influence the progression of uveal melanoma. Conclusions: Long-term effects of LEDs on ocular health cannot be definitively assessed on the basis of current knowledge. Susceptibility to blue light damage varies among the different species. The severity of light-induced retinal damage changes with the time of the day and depends on the diet and genetic background. Additional studies on the safety of long-term exposure to low levels of blue light are needed to determine the safety of LEDs for ocular health. Keywords: blue light – light-emitting diode – macular degeneration – uveal melanoma

Autophagy activated via GRP78 to alleviate endoplasmic reticulum stress for cell survival in blue light-mediated damage of A2E-laden RPEs

BackgroundRetinal pigment epithelium cells (RPEs) are critical for maintaining retinal homeostasis. Accumulation of age-related lipofuscin, N-retinylidene-N-retinylethanolamine (A2E), makes RPEs vulnerable to blue light-mediated damage, which represents an initial cause of some retinal degenerative diseases. This study investigated the activation of autophagy and the signaling pathway involved in glucose-related protein 78 (GRP78) induced autophagy in blue light-mediated damage of A2E-laden RPEs. In addition, we explored whether autophagy could play a protective role by alleviating endoplasmic reticulum (ER) stress to promote RPEs survival.MethodsRPEs were incubated with 25 μM A2E for 2 h and exposed to blue light for 20 min. The expression of ER stress-related apoptotic proteins, CHOP and caspase-12, as well as autophagy marker LC3 were measured by western blot analysis. Autophagosomes were observed by both transmission electron microscopy and immunofluorescence assays. GRP78 interference performed by short hairpin RNA (shRNA) was used to identify the signaling pathway involved in GRP78 induced autophagy. Cell death was assessed using TUNEL analysis.ResultsTreatment with A2E and blue light markedly increased the expression of ER stress-related apoptotic molecules CHOP and caspase-12. The activation of autophagy was recognized by observing autophagosomes at ultrastructural level. Additionally, punctate distributions of LC3 immunofluorescence and enhanced conversions of LC3-I to LC3-II were found in A2E and blue light-treated RPEs. Moreover, GRP78 interference reduced AMPK phosphorylation and promoted mTOR activity, thereby downregulating autophagy. In addition, the inhibition of autophagy made RPEs vulnerable to A2E and blue light damage. In contrast, the autophagy inducer rapamycin alleviated ER stress to promote RPEs survival.ConclusionsGRP78 activates autophagy via AMPK/mTOR in blue light-mediated damage of A2E-laden RPEs in vitro. Autophagy may be a vital endogenous cytoprotective process to alleviate stress for RPEs survival in retinal degenerative diseases.