Potential Phototoxicity of Indocyanine Green in Retinal Pigment Epithelial Cells after Angiography under Ambient Illumination

Indocyanine green (ICG) angiography is an indispensable inspection to diagnose and treat for chorioretinal diseases. In this study, we investigated the phototoxicity of ICG on RPE cells at the levels of residual ICG after angiography under ambient light. After incubation of ARPE-19 cells in a colorless medium containing 0 to 10 μg/mL ICG for 24 hours in the dark or under 2000 lx illumination from a fluorescent lamp, cell viability decreased and cell death rate increased in cultures with more than 5.0 μg/mL ICG under illumination. In culture with 10 μg/mL ICG under illumination, morphology of cells changed to be oval and TUNEL- and malondialdehyde-positive cells increased compared to other cultures with ICG in the dark or without ICG under illumination. Furthermore, the level of intracellular reactive oxygen species was also elevated. On the other hand, toxicity of ICG denatured by illumination was not observed. Blocking green to red light overlapping wavelengths of ICG absorbance exhibited decreased cell death rate. The present study indicated that ICG at the estimated intravenous concentrations after ICG angiography induces potential phototoxicity on human RPE cells via oxidative damage under continuous ambient illumination and that the cytotoxicity is reduced by blocking green to red light wavelengths.

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Nuclear Factor (Erythroid-Derived)-Related Factor 2-Associated Retinal Pigment Epithelial Cell Protection under Blue Light-Induced Oxidative Stress

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/8694641 ◽

2016 ◽

Vol 2016 ◽

pp. 1-9 ◽

Cited By ~ 10

Author(s):

Kei Takayama ◽

Hiroki Kaneko ◽

Keiko Kataoka ◽

Reona Kimoto ◽

Shiang-Jyi Hwang ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Death Rate ◽

Retinal Pigment ◽

Ros Generation ◽

Related Factor ◽

Nuclear Factor ◽

Wild Type ◽

Rpe Cells ◽

Cell Death Rate

Purpose. It is a matter of increasing concern that exposure to light-emitting diodes (LED), particularly blue light (BL), damages retinal cells. This study aimed to investigate the retinal pigment epithelium (RPE) damage caused by BL and to elucidate the role of nuclear factor (erythroid-derived)-related factor 2 (Nrf2) in the pathogenesis of BL-induced RPE damage.Methods. ARPE-19, a human RPE cell line, and mouse primary RPE cells from wild-type andNrf2knockout (Nrf2−/−) mice were cultured under blue LED exposure (intermediate wavelength, 450 nm). Cell death rate and reactive oxygen species (ROS) generation were measured. TUNEL staining was performed to detect apoptosis. Real-time polymerase chain reaction was performed onNRF2mRNA, and western blotting was performed to detect Nrf2 proteins in the nucleus or cytoplasm of RPE cells.Results. BL exposure increased cell death rate and ROS generation in ARPE-19 cells in a time-dependent manner; cell death was caused by apoptosis. Moreover, BL exposure inducedNRF2mRNA upregulation and Nrf2 nuclear translocation in RPE. Cell death rate was significantly higher in RPE cells fromNrf2−/−mice than from wild-type mice.Conclusions. The Nrf2 pathway plays an important role in protecting RPE cells against BL-induced oxidative stress.

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CFH exerts anti-oxidant effects on retinal pigment epithelial cells independently from protecting against membrane attack complex

Scientific Reports ◽

10.1038/s41598-019-50420-9 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 10

Author(s):

Céline Borras ◽

Jérémie Canonica ◽

Sylvie Jorieux ◽

Toufik Abache ◽

Mohamed El Sanharawi ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Epithelial Cells ◽

Retinal Pigment Epithelial ◽

Retinal Pigment ◽

Membrane Attack Complex ◽

Retinal Pigment Epithelial Cells ◽

Rpe Cells ◽

Pigment Epithelial ◽

Pigment Epithelial Cells

Abstract Age Related Macular Degeneration (AMD) is the first cause of social blindness in people aged over 65 leading to atrophy of retinal pigment epithelial cells (RPE), photoreceptors and choroids, eventually associated with choroidal neovascularization. Accumulation of undigested cellular debris within RPE cells or under the RPE (Drusen), oxidative stress and inflammatory mediators contribute to the RPE cell death. The major risk to develop AMD is the Y402H polymorphism of complement factor H (CFH). CFH interacting with oxidized phospholipids on the RPE membrane modulates the functions of these cells, but the exact role of CFH in RPE cell death and survival remain poorly understood. The aim of this study was to analyze the potential protective mechanism of CFH on RPE cells submitted to oxidative stress. Upon exposure to oxidized lipids 4-HNE (4-hydroxy-2-nonenal) derived from photoreceptors, both the human RPE cell line ARPE-19 and RPE cells derived from human induced pluripotent stem cells were protected from death only in the presence of the full length human recombinant CFH in the culture medium. This protective effect was independent from the membrane attack complex (MAC) formation. CFH maintained RPE cells tight junctions’ structure and regulated the caspase dependent apoptosis process. These results demonstrated the CFH anti-oxidative stress functions independently of its capacity to inhibit MAC formation.

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Iron prochelator BSIH protects retinal pigment epithelial cells against cell death induced by hydrogen peroxide

Journal of Inorganic Biochemistry ◽

10.1016/j.jinorgbio.2008.08.001 ◽

2008 ◽

Vol 102 (12) ◽

pp. 2130-2135 ◽

Cited By ~ 33

Author(s):

Louise K. Charkoudian ◽

Tzvete Dentchev ◽

Nina Lukinova ◽

Natalie Wolkow ◽

Joshua L. Dunaief ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Cell Death ◽

Epithelial Cells ◽

Retinal Pigment Epithelial ◽

Retinal Pigment ◽

Retinal Pigment Epithelial Cells ◽

Pigment Epithelial ◽

Pigment Epithelial Cells

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Superoxide Dismutase-1 Induced Oxidative Stress Mediated Apoptosis in Murine Retinal Pigment Epithelial Cells

International Journal of Recent Technology and Engineering - 2 ◽

10.35940/ijrte.d1154.1284s219 ◽

2019 ◽

Vol 8 (4S2) ◽

pp. 463-466

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Vision Loss ◽

Retinal Pigment ◽

Retinal Pigment Epithelial Cells ◽

Age Related Macular Degeneration ◽

Superoxide Dismutase 1 ◽

Central Vision Loss ◽

Age Related ◽

Pigment Epithelial Cells

Age related macular degeneration (AMD) is a complicated ocular disease which occurs in elderly people and leads to central vision loss. The AMD generated because of overproduction of oxidative stress which leads to RPE cell death. The present study investigates whether SOD1 induced MRPE cell death based on that overexpression of SOD1 in MRPE cells which induced cell death. The SOD1 gradually increased ROS production and fragmentation of nuclei. To explore the ER stress persuaded UPR via GRP78, and CHOP, protein expression level analyses were carried out by western blotting. Together, our results represent that SOD1 could possibly produce the oxidant induced MRPE cell death.

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Comparison of organics and heavy metals acute toxicities to Vibrio fischeri

Journal of the Serbian Chemical Society ◽

10.2298/jsc151124011y ◽

2016 ◽

Vol 81 (6) ◽

pp. 697-705 ◽

Cited By ~ 9

Author(s):

Xuepeng Yang ◽

Yan Ji ◽

Fangfang Wang ◽

Jia Xu ◽

Xiangzhen Liu ◽

...

Keyword(s):

Heavy Metals ◽

Cell Death ◽

Benzoic Acid ◽

Death Rate ◽

Vibrio Fischeri ◽

Reaction Times ◽

Inhibition Rate ◽

Cell Death Rate ◽

Bioluminescence Inhibition ◽

The Difference

Vibrio fischeri bioluminescence inhibition has been widely used to test acute toxicities of metals and organics contaminants. However, the differences of metals and organics acute toxicities to V. fischeri have not been compared. Here, four heavy metals (Zn2+, Cu2+, Cd2+, Cr6+) and five organics (phenol, benzoic acid, p-hydroxy benzoic acid, nitro-benzene and benzene) acute toxicities to V. fischeri were investigated. Heavy metals toxicities to V. fischeri were increased along with the reaction time, while the organics toxicities kept the same level in different reaction times. In order to explain the difference, the relative cell death rate of V. fischeri was detected. In metals toxicities tests, the bioluminescence inhibition rate of V. fischeri was found to be significantly higher than the relative cell death rate (P<0.05), while for the organics toxicities tests, the cell death rate was similar to the bioluminescence inhibition rate. These results indicated that organics acute toxicities to V. fischeri could reflect the death of cell, but metals acute toxicities to V. fischeri may not lead to the death of cell, just represent the bioluminescence inhibition.

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Hesperidin Prevents High Glucose-Induced Damage of Retinal Pigment Epithelial Cells

Planta Medica ◽

10.1055/a-0601-7020 ◽

2018 ◽

Vol 84 (14) ◽

pp. 1030-1037 ◽

Cited By ~ 5

Author(s):

Wayne Liu ◽

Shorong-Shii Liou ◽

Tang-Yao Hong ◽

I-Min Liu

Keyword(s):

High Glucose ◽

Retinal Pigment Epithelial ◽

Colorimetric Assay ◽

Retinal Pigment ◽

Retinal Pigment Epithelial Cells ◽

Antioxidant Enzyme Activities ◽

Dependent Manner ◽

Concentration Dependent Manner ◽

Rpe Cells ◽

Pigment Epithelial

AbstractThe present study aimed to determine whether hesperidin, a plant-based active flavanone found in citrus fruits, can prevent high glucose-induced retinal pigment epithelial (RPE) cell impairment. Cultured human RPE cells (ARPE-19) were exposed to a normal glucose concentration (5.5 mM) for 4 d and then soaked in either normal (5.5 mM) or high (33.3 mM) concentrations of D-glucose with or without different concentrations of hesperidin (10, 20, or 40 µM) for another 48 h. The survival rates of the cells were measured using a 3-(4,5-dimethyl thiazol-2-yl)-2,5-diphenyl tetrazolium bromide reduction assay. With the help of a fluorescent probe, the intracellular production of reactive oxygen species (ROS) was evaluated. Colorimetric assay kits were used to assess the antioxidant enzyme activities, and western blotting was used to measure the expression of apoptosis-related protein. Hesperidin was effective in inhibiting high glucose-induced ROS production, preventing loss of cell viability, and promoting the endogenous antioxidant defense components, including glutathione peroxidase, superoxide dismutase, catalase, and glutathione, in a concentration-dependent manner. Furthermore, high glucose triggered cell apoptosis via the upregulation of caspase-9/3, enhancement of cytochrome c release into the cytosol, and subsequent interruption of the Bax/Bcl-2 balance. These detrimental effects were ameliorated by hesperidin in a concentration-dependent manner. We conclude that through the scavenging of ROS and modulation of the mitochondria-mediated apoptotic pathway, hesperidin may protect RPE cells from high glucose-induced injury and thus may be a candidate in preventing the visual impairment caused by diabetic retinopathy.

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Oxidative stress induces ferroptotic cell death in retinal pigment epithelial cells

Experimental Eye Research ◽

10.1016/j.exer.2018.08.019 ◽

2019 ◽

Vol 181 ◽

pp. 316-324 ◽

Cited By ~ 17

Author(s):

Kiyohito Totsuka ◽

Takashi Ueta ◽

Takatoshi Uchida ◽

Murilo F. Roggia ◽

Suguru Nakagawa ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Epithelial Cells ◽

Retinal Pigment Epithelial ◽

Retinal Pigment ◽

Retinal Pigment Epithelial Cells ◽

Pigment Epithelial ◽

Pigment Epithelial Cells

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S-Allylmercapro-N-Acetylcysteine Attenuates the Oxidation-Induced Lens Opacification and Retinal Pigment Epithelial Cell Death In Vitro

Antioxidants ◽

10.3390/antiox8010025 ◽

2019 ◽

Vol 8 (1) ◽

pp. 25 ◽

Cited By ~ 1

Author(s):

Naphtali Savion ◽

Samia Dahamshi ◽

Milana Morein ◽

Shlomo Kotev-Emeth

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Retinal Pigment Epithelial ◽

Retinal Pigment Epithelial Cell ◽

Retinal Pigment ◽

Lens Opacity ◽

Glutathione Level ◽

Rpe Cells ◽

Pigment Epithelial ◽

Lens Opacification

The capacity of S-Allylmercapto-N-acetylcysteine (ASSNAC) to protect human retinal pigment epithelial (RPE) cells (line ARPE-19) and porcine lenses from oxidative stress was studied. Confluent ARPE-19 cultures were incubated with ASSNAC or N-acetyl-cysteine (NAC) followed by exposure to oxidants and glutathione level and cell survival were determined. Porcine lenses were incubated with ASSNAC and then exposed to H2O2 followed by lens opacity measurement and determination of glutathione (reduced (GSH) and oxidized (GSSG)) in isolated lens adhering epithelial cells (lens capsule) and fiber cells consisting the lens cortex and nucleus (lens core). In ARPE-19 cultures, ASSNAC (0.2 mM; 24 h) increased glutathione level by 2–2.5-fold with significantly higher increase in GSH compared to NAC treated cultures. Similarly, ex-vivo exposure of lenses to ASSNAC (1 mM) significantly reduced the GSSG level and prevented H2O2 (0.5 mM)-induced lens opacification. These results demonstrate that ASSNAC up-regulates glutathione level in RPE cells and protects them from oxidative stress-induced cell death as well as protects lenses from oxidative stress-induced opacity. Further validation of these results in animal models may suggest a potential use for ASSNAC as a protective therapy in retinal degenerative diseases as well as in attenuation of oxidative stress-induced lens opacity.

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