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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of bioenergetics and biomembranes 12 (1980), S. 233-247 
    ISSN: 1573-6881
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Heart mitochondria swollen passively in nitrate salts contract in a respiration-dependent reaction which can be attributed to an endogenous cation/H+ exchange component (or components). The rate of contraction increases with increased extent of passive swelling in both Na+ and K+ salts. Since nearly constant internal cation concentrations are maintained during osmotic swelling, this result suggests that both Na+/H+ and K+/H+ exchange is enhanced by increased matrix volume. Endogenous Mg2+ is also lost with increased matrix volume, and this observation, in conjunction with other evidence available in the literature, suggests that monovalent cation/H+ exchanges may be regulated by divalent cations. Passive exchange of Na+/K+,42K+/K+, and24Na+/Na+ can be readily demonstrated in mitochondria swollen in nitrate. All these exchanges are low or not detectable in unswollen control mitochondria, and it appears that they are manifestations of the activated cation/H+ component (or components) functioning in the absence of ΔpH.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of bioenergetics and biomembranes 16 (1984), S. 379-390 
    ISSN: 1573-6881
    Keywords: Quinine ; quinacrine ; mitochondrial K+/H+ antiport ; swelling and contraction of heart mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Physics
    Notes: Abstract Quinine inhibits the respiration-dependent extrusion of K+ from Mg2+-depleted heart mitochondria and the passive osmotic swelling of these mitochondria in K+ and Na+ acetate at alkaline pH. These observations concur with those of Nakashima and Garlid (J. Biol. Chem. 257, 9252, 1982) using rat liver mitochondria. Quinine also inhibits the respiration-dependent contraction of heart mitochondria swollen passively in Na+ or K+ nitrate and the increment of elevated respiration associated with the extrusion of ions from these mitochondria. Quinine, at concentrations up to 0.5 mM, inhibits the respiration-dependent42K+/K+ exchange seen in the presence of mersalyl, but higher levels of the drug produce increased membrane permeability and net K+ loss from the matrix. These results are all consistent with an inhibition of the putative mitochondrial K+/H+ antiport by quinine. However, quinine has other effects on the mitochondrial membrane, and possible alternatives to this interpretation are discussed.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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