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      Prolonged exposures of cerebellar granule neurons to S-nitroso-N-acetylpenicillamine (SNAP) induce neuronal damage independently of peroxynitrite

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      Brain Research
      Elsevier BV

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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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            Reactive oxygen species, antioxidants, and the mammalian thioredoxin system1 1This review is based on the licentiate thesis “Thioredoxin reductase—interactions with the redox active compounds 1-chloro-2,4-dinitrobenzene and lipoic acid” by Jonas Nordberg, 2001, Karolinska Institute, Stockholm, ISBN 91-631-1064-4.

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              Oxidative stress, glutamate, and neurodegenerative disorders

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                Author and article information

                Journal
                Brain Research
                Brain Research
                Elsevier BV
                00068993
                September 2008
                September 2008
                : 1230
                :
                : 265-272
                Article
                10.1016/j.brainres.2008.06.109
                8f27e97f-2c1f-4edc-8d7d-b1e508379814
                © 2008

                http://www.elsevier.com/tdm/userlicense/1.0/

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