We are analyzing https://link.springer.com/article/10.1186/1471-2202-9-4.

Title:
Differential production of superoxide by neuronal mitochondria | BMC Neuroscience
Description:
Background Mitochondrial DNA (mtDNA) mutations, which are present in all mitochondria-containing cells, paradoxically cause tissue-specific disease. For example, Leber
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Keywords {🔍}

mitochondria, superoxide, rgc, cells, production, complex, mitochondrial, cerebral, cell, metc, article, neuroblastoma, protein, rgcs, levels, compared, mutations, isolated, undifferentiated, pubmed, lhon, differences, substrate, similar, google, scholar, differentiated, components, iii, table, presence, figure, expression, samples, line, succinate, lower, inhibitor, antimycin, full, mtdna, cas, content, optic, size, increase, neuronal, neuropathy, rotenone, death,

Topics {✒️}

real-time quantitative pcr quantitative real-time pcr real-time rt-pcr open access article voltage-dependent anion channel step rt-pcr kit adult long-evans rats full size image time-lapse fluorescent baseline cell type-specific handling mitochondrial-derived intracellular messenger article download pdf mitochondrial dna complex inherited mtdna abnormalities antioxid redox signal reduced redox state central neuron contained glucose-deficient galactose media nmol/min/mg protein 004 nmol/min/mg protein rt-pcr data retina research foundation full access cell type-specific differences authors’ original file privacy choices/manage cookies kinase-dependent differentiation induces mitochondrial dysfunction hereditary optic neuropathy rt-pcr analysis experience apoptotic death including mitochondrial encephalomyopathy mitochondrial superoxide production compared mitochondrial isolates equal size area complexes i-iv complex-specific metc substrates cell-types correlated mitochondrial superoxide dismutase canada research chair mitochondrial isolation kit retinal ganglion cells mitochondrial free sulfhydryls standardized mitochondrial preparations optic neuropathy induced mitochondrial superoxide levels mitochondrial protein shows basal superoxide production mitotracker green fm produce differential purification

Questions {❓}

But why would abnormalities in superoxide production be a mechanism for the relatively specific effect of LHON mtDNA mutations on RGCs?

Schema {🗺️}

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         headline:Differential production of superoxide by neuronal mitochondria
         description:Mitochondrial DNA (mtDNA) mutations, which are present in all mitochondria-containing cells, paradoxically cause tissue-specific disease. For example, Leber's hereditary optic neuropathy (LHON) results from one of three point mutations mtDNA coding for complex I components, but is only manifested in retinal ganglion cells (RGCs), a central neuron contained within the retina. Given that RGCs use superoxide for intracellular signaling after axotomy, and that LHON mutations increase superoxide levels in non-RGC transmitochondrial cybrids, we hypothesized that RGCs regulate superoxide levels differently than other neuronal cells. To study this, we compared superoxide production and mitochondrial electron transport chain (METC) components in isolated RGC mitochondria to mitochondria isolated from cerebral cortex and neuroblastoma SK-N-AS cells. In the presence of the complex I substrate glutamate/malate or the complex II substrate succinate, the rate of superoxide production in RGC-5 cells was significantly lower than cerebral or neuroblastoma cells. Cerebral but not RGC-5 or neuroblastoma cells increased superoxide production in response to the complex I inhibitor rotenone, while neuroblastoma but not cerebral or RGC-5 cells dramatically decreased superoxide production in response to the complex III inhibitor antimycin A. Immunoblotting and real-time quantitative PCR of METC components demonstrated different patterns of expression among the three different sources of neuronal mitochondria. RGC-5 mitochondria produce superoxide at significantly lower rates than cerebral and neuroblastoma mitochondria, most likely as a result of differential expression of complex I components. Diversity in METC component expression and function could explain tissue specificity in diseases associated with inherited mtDNA abnormalities.
         datePublished:2008-01-08T00:00:00Z
         dateModified:2008-01-08T00:00:00Z
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            Superoxide Production
            Mitochondrial Electron Transport Chain
            Increase Superoxide Production
            Mitochondrial Superoxide Production
            Lithium Dodecyl Sulfate
            Neurosciences
            Neurobiology
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      headline:Differential production of superoxide by neuronal mitochondria
      description:Mitochondrial DNA (mtDNA) mutations, which are present in all mitochondria-containing cells, paradoxically cause tissue-specific disease. For example, Leber's hereditary optic neuropathy (LHON) results from one of three point mutations mtDNA coding for complex I components, but is only manifested in retinal ganglion cells (RGCs), a central neuron contained within the retina. Given that RGCs use superoxide for intracellular signaling after axotomy, and that LHON mutations increase superoxide levels in non-RGC transmitochondrial cybrids, we hypothesized that RGCs regulate superoxide levels differently than other neuronal cells. To study this, we compared superoxide production and mitochondrial electron transport chain (METC) components in isolated RGC mitochondria to mitochondria isolated from cerebral cortex and neuroblastoma SK-N-AS cells. In the presence of the complex I substrate glutamate/malate or the complex II substrate succinate, the rate of superoxide production in RGC-5 cells was significantly lower than cerebral or neuroblastoma cells. Cerebral but not RGC-5 or neuroblastoma cells increased superoxide production in response to the complex I inhibitor rotenone, while neuroblastoma but not cerebral or RGC-5 cells dramatically decreased superoxide production in response to the complex III inhibitor antimycin A. Immunoblotting and real-time quantitative PCR of METC components demonstrated different patterns of expression among the three different sources of neuronal mitochondria. RGC-5 mitochondria produce superoxide at significantly lower rates than cerebral and neuroblastoma mitochondria, most likely as a result of differential expression of complex I components. Diversity in METC component expression and function could explain tissue specificity in diseases associated with inherited mtDNA abnormalities.
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         Mitochondrial Electron Transport Chain
         Increase Superoxide Production
         Mitochondrial Superoxide Production
         Lithium Dodecyl Sulfate
         Neurosciences
         Neurobiology
         Animal Models
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