Cd2+ effects on respiration and swelling of rat liver mitochondria were modified by monovalent cations

Changes in Cd2+ effects on respiration of succinate-energized rat liver mitochondria were studied after replacement of 100 mM KCl in an incubation medium by equimolar amounts of NaCl or LiCl, or by 200 mM sucrose. In KCl medium, 2.5-10 microM Cd2+ decreased the state 3 and 2,4-dinitrophenol (DNP)-st...

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Veröffentlicht in:Journal of inorganic biochemistry 1998-04, Vol.70 (1), p.17-23
Hauptverfasser: Korotkov, S M, Skulskii, I A, Glazunov, V V
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Sprache:eng
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Zusammenfassung:Changes in Cd2+ effects on respiration of succinate-energized rat liver mitochondria were studied after replacement of 100 mM KCl in an incubation medium by equimolar amounts of NaCl or LiCl, or by 200 mM sucrose. In KCl medium, 2.5-10 microM Cd2+ decreased the state 3 and 2,4-dinitrophenol (DNP)-stimulated respiration of mitochondria, and increased their respiration in the state 4, however, 10-40 microM Cd2+ diminished the state 4 respiration. Compared to the experiments with KCl medium, it was demonstrated that Cd2+ effects on the mitochondrial respiration was increased in NaCl medium, decreased in sucrose medium, and unchanged in LiCl medium, except that 10-25 microM Cd2+ decreased the state 4 respiration of mitochondria in the same way as in the NaCl medium. Cd2+ (20 microM) stimulated an extensive swelling of nonenergized mitochondria incubated in 125 mM nitrate media, the effect being increased in the series of Li < Na < K < NH4. Swelling of succinate-energized mitochondria incubated in K-acetate medium was additionally stimulated by 10 microM Cd2+. The initially low swelling of succinate-energized mitochondria in the KCl medium increased with increase in Cd2+ concentrations in this medium. Differences found in the Cd2+ effects on respiration and on swelling of mitochondria incubated in the media used are discussed in terms of general ion permeabilities and differences in Cd2+ binding, its uptake, and interaction with respiratory enzymes.
ISSN:0162-0134
DOI:10.1016/S0162-0134(98)00008-7