Oxidative damage is a potential cause of cone cell death in retinitis pigmentosa

2005 ◽  
Vol 203 (3) ◽  
pp. 457-464 ◽  
Author(s):  
JiKui Shen ◽  
Xiaoru Yang ◽  
Aling Dong ◽  
Robert M. Petters ◽  
You-Wei Peng ◽  
...  
Keyword(s):  
Cell Death ◽  
Oxidative Damage ◽  
Retinitis Pigmentosa ◽  
Cone Cell

scholarly journals Increased Expression of Catalase and Superoxide Dismutase 2 Reduces Cone Cell Death in Retinitis Pigmentosa

2009 ◽  
Vol 17 (5) ◽  
pp. 778-786 ◽  
Author(s):  
Shinichi Usui ◽  
Keiichi Komeima ◽  
Sun Young Lee ◽  
Young-Joon Jo ◽  
Shinji Ueno ◽  
...  
Keyword(s):  
Cell Death ◽  
Superoxide Dismutase ◽  
Retinitis Pigmentosa ◽  
Cone Cell ◽  
Superoxide Dismutase 2

scholarly journals Antioxidants reduce cone cell death in a model of retinitis pigmentosa

2006 ◽  
Vol 103 (30) ◽  
pp. 11300-11305 ◽  
Author(s):  
K. Komeima ◽  
B. S. Rogers ◽  
L. Lu ◽  
P. A. Campochiaro
Keyword(s):  
Cell Death ◽  
Retinitis Pigmentosa ◽  
Cone Cell

scholarly journals Gypenosides Alleviate Cone Cell Death in a Zebrafish Model of Retinitis Pigmentosa

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1050
Author(s):  
Xing Li ◽  
Reem Hasaballah Alhasani ◽  
Yanqun Cao ◽  
Xinzhi Zhou ◽  
Zhiming He ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinitis Pigmentosa ◽  
Network Pharmacology ◽  
Genetic Abnormality ◽  
Hub Genes ◽  
Zebrafish Model ◽  
Cone Cell ◽  
Antioxidant Genes ◽  
Rod Cells ◽  
Cone Cells

Retinitis pigmentosa (RP) is a group of visual disorders caused by mutations in over 70 genes. RP is characterized by initial degeneration of rod cells and late cone cell death, regardless of genetic abnormality. Rod cells are the main consumers of oxygen in the retina, and after the death of rod cells, the cone cells have to endure high levels of oxygen, which in turn leads to oxidative damage and cone degeneration. Gypenosides (Gyp) are major dammarane-type saponins of Gynostemma pentaphyllum that are known to reduce oxidative stress and inflammation. In this project we assessed the protective effect of Gyp against cone cell death in the rpgrip1 mutant zebrafish, which recapitulate the classical pathological features found in RP patients. Rpgrip1 mutant zebrafish were treated with Gyp (50 µg/g body weight) from two-months post fertilization (mpf) until 6 mpf. Gyp treatment resulted in a significant decrease in cone cell death compared to that of untreated mutant zebrafish. A markedly low level of reactive oxygen species and increased expression of antioxidant genes were detected in Gyp-incubated mutant zebrafish eyes compared to that of untreated mutant zebrafish. Similarly, the activities of catalase and superoxide dismutase and the level of glutathione were significantly increased in Gyp-treated mutant zebrafish eyes compared to that of untreated mutant zebrafish. Gyp treatment also decreased endoplasmic reticulum stress in rpgrip1 mutant eyes. Expression of proinflammatory cytokines was also significantly decreased in Gyp-treated mutant zebrafish eyes compared to that of untreated mutant zebrafish. Network pharmacology analysis demonstrated that the promotion of cone cell survival by Gyp is possibly mediated by multiple hub genes and associated signalling pathways. These data suggest treatment with Gyp will benefit RP patients.

The mechanism of cone cell death in Retinitis Pigmentosa

2018 ◽  
Vol 62 ◽  
pp. 24-37 ◽  
Author(s):  
Peter A. Campochiaro ◽  
Tahreem A. Mir
Keyword(s):  
Cell Death ◽  
Retinitis Pigmentosa ◽  
Cone Cell

scholarly journals Blockade of neuronal nitric oxide synthase reduces cone cell death in a model of retinitis pigmentosa

2008 ◽  
Vol 45 (6) ◽  
pp. 905-912 ◽  
Author(s):  
Keiichi Komeima ◽  
Shinichi Usui ◽  
Jikui Shen ◽  
Brian S. Rogers ◽  
Peter A. Campochiaro
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Nitric Oxide Synthase ◽  
Retinitis Pigmentosa ◽  
Neuronal Nitric Oxide Synthase ◽  
Cone Cell ◽  
Oxide Synthase

scholarly journals NADPH oxidase plays a central role in cone cell death in retinitis pigmentosa

2009 ◽  
Vol 110 (3) ◽  
pp. 1028-1037 ◽  
Author(s):  
Shinichi Usui ◽  
Brian C. Oveson ◽  
Sun Young Lee ◽  
Young-Joon Jo ◽  
Tsunehiko Yoshida ◽  
...  
Keyword(s):  
Cell Death ◽  
Retinitis Pigmentosa ◽  
Nadph Oxidase ◽  
Cone Cell

Glial cytotoxicity of low doses of cadmium as a model of heavy metal pollution influence on vertebrates

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oxidative Damage ◽  
Cadmium Chloride ◽  
Glioma Cells ◽  
Low Doses ◽  
Genotoxic Effects ◽  
Cadmium Ions

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.

scholarly journals Pharmaceutical Induction of PGC-1α Promotes Retinal Pigment Epithelial Cell Metabolism and Protects against Oxidative Damage

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Sangeeta Satish ◽  
Hannah Philipose ◽  
Mariana Aparecida Brunini Rosales ◽  
Magali Saint-Geniez
Keyword(s):  
Cell Death ◽  
Antioxidant Enzymes ◽  
Oxidative Damage ◽  
Therapeutic Potential ◽  
Retinal Pigment Epithelial Cell ◽  
Cell Metabolism ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Age Related Macular Degeneration ◽  
Age Related

Retinal pigment epithelium (RPE) dysfunction due to accumulation of reactive oxygen species and oxidative damage is a key event in the development of age-related macular degeneration (AMD). Here, we examine the therapeutic potential of ZLN005, a selective PGC-1α transcriptional regulator, in protecting RPE from cytotoxic oxidative damage. Gene expression analysis on ARPE-19 cells treated with ZLN005 shows robust upregulation of PGC-1α and its associated transcription factors, antioxidant enzymes, and mitochondrial genes. Energetic profiling shows that ZLN005 treatment enhances RPE mitochondrial function by increasing basal and maximal respiration rates, and spare respiratory capacity. In addition, ZLN005 robustly protects ARPE-19 cells from cell death caused by H2O2, ox-LDL, and NaIO3 without exhibiting any cytotoxicity under basal conditions. ZLN005 protection against H2O2-mediated cell death was lost in PGC-1α-silenced cells. Our data indicates that ZLN005 efficiently protects RPE cells from oxidative damage through selective induction of PGC-1α and its target antioxidant enzymes. ZLN005 may serve as a novel therapeutic agent for retinal diseases associated with RPE dystrophies.

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