The Experts below are selected from a list of 78 Experts worldwide ranked by ideXlab platform
Pier Luigi San Biagio - One of the best experts on this subject based on the ideXlab platform.
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Are oxidative stress and mitochondrial dysfunction the key players in the neurodegenerative diseases
Free radical research, 2012Co-Authors: Marta Di Carlo, Daniela Giacomazza, Pasquale Picone, Domenico Nuzzo, Pier Luigi San BiagioAbstract:Oxidative stress has long been linked to neuronal cell death that is associated with certain neurodegenerative conditions. Whether it is a primary cause or merely a Downstream Consequence of the neurodegenerative and aging process is still an open question. Mitochondria are deeply involved in the production of reactive oxygen species through the electron carriers of the respiratory chain and their role in neurodegenerative diseases is discussed here. Moreover, the input of new technological approaches in the study of oxidative stress response or in the evidence of an oxidative stress component in neurodegeneration is reviewed in this paper.
William J. Nicklas - One of the best experts on this subject based on the ideXlab platform.
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Oxidative stress during energy impairment in mesencephalic cultures is not a Downstream Consequence of a secondary excitotoxicity.
Neuroscience, 2000Co-Authors: Gail D. Zeevalk, Laura P. Bernard, William J. NicklasAbstract:Abstract Past studies have shown that inhibiting energy metabolism with malonate in mesencephalic cultures damages neurons by mechanisms involving N -methyl- d -aspartate receptors and free radicals. Overstimulation of N -methyl- d -aspartate receptors is known to produce free radicals. This study was, therefore, carried out to determine if N -methyl- d -aspartate receptor activation triggered by energy impairment was a significant contributor to the oxidative stress generated during energy inhibition. Exposure of mesencephalic cultures to malonate for the minimal time required to produce toxicity, i.e. 6 h, resulted in an increase in the efflux of both oxidized and reduced glutathione, and a decrease in tissue levels of reduced glutathione. In contrast, exposure to 1 mM glutamate for 1 h caused an increased efflux of reduced glutathione, but no changes in intra- or extracellular oxidized glutathione or intracellular reduced glutathione. Blocking N -methyl- d -aspartate receptors with MK-801 (0.5 μM) during malonate exposure did not modify malonate-induced alterations in glutathione status or free radical generation as monitored by dihydrochlorofluorescein diacetate and dihydrorhodamine 123 fluorescence. In contrast, the increase in dihydrorhodamine fluorescence caused by glutamate was completely blocked by MK-801. Reduction of tissue glutathione with a 24 h pretreatment with 10 μM buthionine sulfoxamine, as shown previously, greatly potentiated malonate-induced toxicity to dopamine and GABA neurons, but had no potentiating effect on toxicity due to glutamate. The findings indicate that although oxidative stress mediates damage due either to energy deprivation or excitotoxicity, N -methyl- d -aspartate receptor over-stimulation does not contribute significantly to the oxidative stress that is incurred during malonate exposure.
Marta Di Carlo - One of the best experts on this subject based on the ideXlab platform.
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Are oxidative stress and mitochondrial dysfunction the key players in the neurodegenerative diseases
Free radical research, 2012Co-Authors: Marta Di Carlo, Daniela Giacomazza, Pasquale Picone, Domenico Nuzzo, Pier Luigi San BiagioAbstract:Oxidative stress has long been linked to neuronal cell death that is associated with certain neurodegenerative conditions. Whether it is a primary cause or merely a Downstream Consequence of the neurodegenerative and aging process is still an open question. Mitochondria are deeply involved in the production of reactive oxygen species through the electron carriers of the respiratory chain and their role in neurodegenerative diseases is discussed here. Moreover, the input of new technological approaches in the study of oxidative stress response or in the evidence of an oxidative stress component in neurodegeneration is reviewed in this paper.
Steven R Blanke - One of the best experts on this subject based on the ideXlab platform.
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Cellular Vacuolation and Mitochondrial Cytochrome c Release Are Independent Outcomes of Helicobacter pylori Vacuolating Cytotoxin Activity That Are Each Dependent on Membrane Channel Formation
Journal of Biological Chemistry, 2003Co-Authors: David C. Willhite, Timothy L. Cover, Steven R BlankeAbstract:Abstract Helicobacter pylori vacuolating toxin (VacA) is a secreted toxin that is reported to produce multiple effects on mammalian cells. In this study, we explored the relationship between VacA-induced cellular vacuolation and VacA-induced cytochrome c release from mitochondria. Within intoxicated cells, vacuolation precedes cytochrome c release and occurs at lower VacA concentrations, indicating that cellular vacuolation is not a Downstream Consequence of cytochrome c release. Conversely, bafilomycin A1 blocks VacA-induced vacuolation but not VacA-induced cytochrome c release, which indicates that cytochrome c release is not a Downstream Consequence of cellular vacuolation. Acid activation of purified VacA is required for entry of VacA into cells, and correspondingly, acid activation of the toxin is required for both vacuolation and cytochrome c release, which suggests that VacA must enter cells to produce these two effects. Single amino acid substitutions (P9A and G14A) that ablate vacuolating activity and membrane channel-forming activity render VacA unable to induce cytochrome c release. Channel blockers known to inhibit cellular vacuolation and VacA membrane channel activity also inhibit cytochrome c release. These data indicate that cellular vacuolation and mitochondrial cytochrome c release are two independent outcomes of VacA intoxication and that both effects are dependent on the formation of anion-selective membrane channels.
Lin L. Mantell - One of the best experts on this subject based on the ideXlab platform.
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Hyperoxia in cell culture. A non-apoptotic programmed cell death.
Annals of the New York Academy of Sciences, 1999Co-Authors: Jeffrey A. Kazzaz, Stuart Horowitz, Lin L. MantellAbstract:Here we discuss the morphological features and our current understanding of the pathways involved in non-apoptotic cell death from O2 toxicity. Preliminary data on hyperoxic signaling indicate that NF-kappa B translocation (and presumptive activation) is not a result of the p42/p44 MAPK pathway, but a likely Downstream Consequence of activation of the JNK pathway. Our observations suggest the existence of multiple signal transduction pathways in hyperoxia-induced cell death: one involved in the stress response which appears to be NF-kappa B-dependent and another in cell death.
