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      Mitochondria as Potential Targets and Initiators of the Blue Light Hazard to the Retina

      review-article
      1 , 2 , 1 , 2 , 1 ,
      Oxidative Medicine and Cellular Longevity
      Hindawi

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          Abstract

          Commercially available white light-emitting diodes (LEDs) have an intense emission in the range of blue light, which has raised a range of public concerns about their potential risks as retinal hazards. Distinct from other visible light components, blue light is characterized by short wavelength, high energy, and strong penetration that can reach the retina with relatively little loss in damage potential. Mitochondria are abundant in retinal tissues, giving them relatively high access to blue light, and chromophores, which are enriched in the retina, have many mitochondria able to absorb blue light and induce photochemical effects. Therefore, excessive exposure of the retina to blue light tends to cause ROS accumulation and oxidative stress, which affect the structure and function of the retinal mitochondria and trigger mitochondria-involved death signaling pathways. In this review, we highlight the essential roles of mitochondria in blue light-induced photochemical damage and programmed cell death in the retina, indicate directions for future research and preventive targets in terms of the blue light hazard to the retina, and suggest applying LED devices in a rational way to prevent the blue light hazard.

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          Mitochondrial dynamics and apoptosis.

          In healthy cells, mitochondria continually divide and fuse to form a dynamic interconnecting network. The molecular machinery that mediates this organelle fission and fusion is necessary to maintain mitochondrial integrity, perhaps by facilitating DNA or protein quality control. This network disintegrates during apoptosis at the time of cytochrome c release and prior to caspase activation, yielding more numerous and smaller mitochondria. Recent work shows that proteins involved in mitochondrial fission and fusion also actively participate in apoptosis induction. This review will cover the recent advances and presents competing models on how the mitochondrial fission and fusion machinery may intersect apoptosis pathways.
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            Mediation of poly(ADP-ribose) polymerase-1-dependent cell death by apoptosis-inducing factor.

            Poly(ADP-ribose) polymerase-1 (PARP-1) protects the genome by functioning in the DNA damage surveillance network. PARP-1 is also a mediator of cell death after ischemia-reperfusion injury, glutamate excitotoxicity, and various inflammatory processes. We show that PARP-1 activation is required for translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus and that AIF is necessary for PARP-1-dependent cell death. N-methyl-N'-nitro-N-nitrosoguanidine, H2O2, and N-methyl-d-aspartate induce AIF translocation and cell death, which is prevented by PARP inhibitors or genetic knockout of PARP-1, but is caspase independent. Microinjection of an antibody to AIF protects against PARP-1-dependent cytotoxicity. These data support a model in which PARP-1 activation signals AIF release from mitochondria, resulting in a caspase-independent pathway of programmed cell death.
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              Mitochondrial DNA damage is more extensive and persists longer than nuclear DNA damage in human cells following oxidative stress

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                Author and article information

                Contributors
                Journal
                Oxid Med Cell Longev
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Hindawi
                1942-0900
                1942-0994
                2019
                21 August 2019
                : 2019
                : 6435364
                Affiliations
                1Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China
                2Department of Clinical Medicine, The Second Clinical Medical College, Nanchang University, Nanchang 330006, China
                Author notes

                Academic Editor: Mario Zoratti

                Author information
                https://orcid.org/0000-0001-6622-9674
                Article
                10.1155/2019/6435364
                6721470
                31531186
                5aaf8c14-28a8-42b4-a20c-060a7eedef10
                Copyright © 2019 Jin-Xin Tao et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 31 March 2019
                : 18 June 2019
                : 25 July 2019
                Funding
                Funded by: National Natural Science Foundation of China
                Award ID: 81760446
                Award ID: 81660420
                Funded by: Natural Science Foundation of Jiangxi Province
                Award ID: 20171ACB20035
                Funded by: Construction Plan of the Superior Science and Technology Innovation Team of Jiangxi Province
                Award ID: 20152BCB24009
                Funded by: Foreign Science and Technology Cooperation Plan of Jiangxi Province
                Award ID: 20151BDH80009
                Categories
                Review Article

                Molecular medicine
                Molecular medicine

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