ArticleEye (London, England)2014
Melatonin and amfenac modulate calcium entry, apoptosis, and oxidative stress in ARPE-19 cell culture exposed to blue light irradiation (405 nm).
Article in Eye (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 39 citations in OpenAlex.
- Inhibition of oxidative stress-induced epithelial-mesenchymal transition in retinal pigment epithelial cells of age-related macular degeneration model by suppressing ERK activation.Journal of advanced research · 2024Article
- Adverse effect propensity: A new feature of Gulf War illness predicted by environmental exposures.iScience · 2023Article
- Selenium Protects ARPE-19 and ACBRI 181 Cells against High Glucose-Induced Oxidative Stress.Molecules (Basel, Switzerland) · 2023Article
- Calcium acts as a central player in melatonin antitumor activity in sarcoma cells.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Bevacizumab induces oxidative cytotoxicity and apoptosis via TRPM2 channel activation in retinal pigment epithelial cells: Protective role of glutathione.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2021Article
- Antioxidant Role of PRGF on RPE Cells after Blue Light Insult as a Therapy for Neurodegenerative Diseases.International journal of molecular sciences · 2020Article
- Autophagy in Age-Related Macular Degeneration: A Regulatory Mechanism of Oxidative Stress.Oxidative medicine and cellular longevity · 2020Review
- Mitochondria as Potential Targets and Initiators of the Blue Light Hazard to the Retina.Oxidative medicine and cellular longevity · 2019Review
- Protective Effect of Melatonin against Oxidative Stress-Induced Apoptosis and Enhanced Autophagy in Human Retinal Pigment Epithelium Cells.Oxidative medicine and cellular longevity · 2018Article
- Mitochondrial Fission Is Required for Blue Light-Induced Apoptosis and Mitophagy in Retinal Neuronal R28 Cells.Frontiers in molecular neuroscience · 2018Article
- Light and the City: Breast Cancer Risk Factors Differ Between Urban and Rural Women in Israel.Integrative cancer therapies · 2017Article
- Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment.Oncotarget · 2016Review
- A novel AhR ligand, 2AI, protects the retina from environmental stress.Scientific reports · 2016Article
- Increased Expression of Transient Receptor Potential Vanilloid 4 in Cortical Lesions of Patients with Focal Cortical Dysplasia.CNS neuroscience & therapeutics · 2016Article
- Reduction in traumatic brain injury-induced oxidative stress, apoptosis, and calcium entry in rat hippocampus by melatonin: Possible involvement of TRPM2 channels.Metabolic brain disease · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeUnder conditions of oxidative stress, cell apoptosis is triggered through the mitochondrial intrinsic pathway. Increased levels of reactive oxygen species (ROS) are linked to excess cell loss and mediate the initiation of apoptosis in a diverse range of cell types. The aims of this study were to assess intracellular Ca(2+) release, ROS production, and caspase-3, and -9 activation in ARPE-19 cells during the blue light-mediated cell death, and to examine a potential protective effect of melatonin and amfenac, in the apoptotic cascade.
methodsARPE-19 cells were cultured in their medium. First, MTT tests were performed to determine the protective effects of amfenac and melatonin. Cells were then exposed to blue light irradiation in an incubator. Intracellular Ca(2+) release experiments, mitochondrial membrane depolarization, apoptosis assay, glutathione (GSH), glutathione peroxidase (GSH-Px), and ROS experiments were done according to the method stated in the Materials and methods section.
resultsCell death was clearly associated with increased levels of ROS production, as measured by 2',7'-dichlorofluorescein fluorescence, and associated increase in Ca(2+) levels, as measured by Fura-2-AM. Blue light-induced cell death was associated with an increased level of caspase-3 and 9, suggesting mediation via the apoptotic pathway. Cell death was also associated with mitochondrial depolarization. Melatonin was shown to delay these three steps.
conclusionMelatonin, amfenac, and their combination protect ARPE-19 cells against blue light-triggered ROS accumulation and caspase-3 and -9 activation. The antiapoptotic effect of melatonin and amfenac at doses inhibiting caspase synthesis modified Ca(2+) release and prevented excessive ROS production, suggesting a new therapeutic approach to age-related macular degeneration.
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