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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 111 (1992), S. 11-15 
    ISSN: 1573-4919
    Keywords: superoxide dismutase ; oxidative stress ; toxicology ; calcium fluxes ; free radicals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Incubation of freshly isolated rat liver mitochondria in the presence of oxygen free radical generating hypoxanthine —xanthine oxidase system led to swelling of mitochondria as measured by the change in optical density, which was reversed by the addition of superoxide dismutase. O2 − in the presence of CaCl2 enhanced the peroxidative decomposition of mitochondrial membrane lipids along with swelling of the organelle. Free radical generation led to enhancement of monoamine oxidase activity while glutathione peroxidase and cytochrome c oxidase were inhibited. Tertbutyl hydroperoxide (t-BHP) caused mitochondrial swelling through oxidative stress. Incorporation of ruthenium red, which is a Ca2+ transport blocker, during assay abolished peroxidative membrane damage and swelling. Dithiothreitol (DTT) accorded protection against t-BHP induced mitochondrial swelling. The above in vitro data suggest a possible interrelationship of active oxygen species, membrane damage and calcium dynamics.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 124 (1993), S. 101-106 
    ISSN: 1573-4919
    Keywords: mitochondrial swelling ; lipid peroxidation ; Ca functions ; biological response modifiers ; free radicals
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In order to understand any involvement of altered calcium functions in peroxidative membrane damage, the effect of a few chemicals, known to modify specific biological responses involving calcium related functions on mitochondrial swellingin vitro was studied. Histamine caused swelling, whereas antihistamines reduced calcium induced swelling. Anti-inflammatory agents aspirin and indomethacin did not affect the initial rapid phase of swelling but reduced the swelling during the later phase. The uncouplers of oxidative phosphorylation and electron transport chain blockers such as dinitrophenol (DNP), antimycin-A and rotenone reduced swelling and the respiratory inhibitors KCN and sodium azide completely abolished it. Trifluoperazine, an anti-calmodulin agent did not influence the initial phase of calcium induced swelling but in the subsequent phase swelling was reduced. c-AMP as well as calcium ionophores, calcimycin and lasalocid acid, potentiated swelling. Thus agents capable of modulating calcium functions could influence thein vitro swelling of mitochondria.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Molecular and cellular biochemistry 154 (1996), S. 39-45 
    ISSN: 1573-4919
    Keywords: free radicals ; oxidative stress ; mitochondrial swelling ; tert-butyl hydroperoxide ; calcium deregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Tert-butyl hydroperoxide induced swelling of freshly isolated rat liver mitochondria was inhibited by butylated hydroxytoluene, butylated hydroxyanisole and α-tocopherol by acting at the initial phase. EDTA was more effective than EGTA in reducing the initial swelling and so were desferal and bipyrridyl. Spermine, an allosteric activator of calcium uptake, enhanced swelling whereas lanthanum and ruthenium red, the Ca2+ uniport blockers, reduced it. Inhibition of phospholipase A2 by dibucaine and Ca2+ activated proteases by antipain and leupeptin also reduced t-BHP induced swelling. The data indicate that peroxidative mitochondrial swelling involves an iron mediated initial rapid phase and a subsequent calcium dependent propagation phase.
    Type of Medium: Electronic Resource
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