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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 388 (1980), S. 217-220 
    ISSN: 1432-2013
    Keywords: Calcium ionophore ; A23187 ; Epithelial transport ; Toad urinary bladder ; Oxidative phosphorylation ; Oxygen consumption ; Cell viability
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The divalent cation ionophore A23187 increased oxygen consumption by isolated epithelial cells from toad urinary bladder, an increase similar to that seen with 2,4-dinitrophenol, a classic uncoupler of mitochondrial oxidative phosphorylation. This respiratory stimulation was not seen in calcium-free incubation media. That this A23187 induced rise in cell oxygen consumption was due to a primary uncoupling action on mitochondrial oxidative phosphorylation rather than secondary to stimulation of cellular transport processes and mediated via increased cellular ADP levels was suggested by the ability of A23187 to release the inhibition of cellular respiration by oligomycin, an inhibitor of the mitochondrial proton ATPase which blocks the stimulation of mitochondrial respiration by ADP. Since active transepithelial ion transport and cellular energy production are closely linked processes, the uncoupling action of A23187 in the presence of extracellular calcium is sufficient to account for an acute decline in active ion transport across epithelia without invoking other calcium-mediated processes. Furthermore, isolated epithelial cells exposed to A23187 for 90 min had greater than 50% loss of viability, as measured by failure of Trypan blue exclusion. The subacute A23187 induced declines in transepithelial transport, therefore, may be secondary to its non-specific effects on cell viability.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation 15 (1991), S. 291-301 
    ISSN: 1573-2576
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent evidence indicates that under in vitro conditions, superoxide anion and hydrogen peroxide (H2O2) are unstable in the presence of manganese ion (Mn2+). The current studies snow that in the presence of Mn2+, H2O2-mediated injury of endothelial cells is greatly attenuated. A source of bicarbonate ion and amino acid is required for Mn2+ to exert its protective effects. Injury by phorbol ester-activated neutrophils is also attenuated under the same conditions. EDTA reverses the protective effects. Acute lung injury produced in vivo in rats by intratracheal instillation of glucose-glucose oxidase is almost completely blocked in rats treated with Mn2+ and glycine. Conversely, treatment of rats with EDTA, a chelator of Mn2+, markedly accentuates lung injury caused by glucose-glucose oxidase. These data are consistent with the findings of others that Mn2+ can facilitate direct oxidation of amino acids with concomitant H2O2 disproportionation. This could form the basis of a new therapeutic approach against oxygen radical-mediated tissue injury.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    ISSN: 1553-4006
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Notes: Loss of Ca2+ homeostasis, often in the form of cytoplasmic increases, leads to cell injury. Depending upon cell type and the intensity of Ca2+ toxicity, the ensuing pathology can be reversible or irreversible. Although multiple destructive processes are activated by Ca2+, lethal outcomes are determined largely by Ca2+-induced mitochondrial permeability transition. This form of damage is primarily dependent upon mitochondrial Ca2+ accumulation, which is regulated by the mitochondrial membrane potential. Retention of the mitochondrial membrane potential during Ca2+ increases favors mitochondrial Ca2+ uptake and overload, resulting in mitochondrial permeability transition and cell death. In contrast, dissipation of mitochondrial membrane potential reduces mitochondrial Ca2+ uptake, retards mitochondrial permeability transition, and delays death, even in cells with large Ca2+ increases. The rates of mitochondrial membrane potential dissipation and mitochondrial Ca2+ uptake may determine cellular sensitivity to Ca2+ toxicity under pathological conditions, including ischemic injury.
    Type of Medium: Electronic Resource
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