Calcium transport in mitochondria

Selwyn, Michael J.; Dawson, Alan P.; Dunnett, S. Jane

doi:10.1016/0014-5793(70)80402-1

Cited by 141 publications

(47 citation statements)

References 14 publications

(7 reference statements)

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“…Evidence for the electrogenic nature of Ca" influx was provided by the observation of Selwyn et al [28] that Ca2+ influx can be driven by a diffusion produced by a gradient of H' (in the presence of an uncoupler to permit electrogenic H + permeation) or of SCN-, and by Scarpa and Azzone [29] who uses K + in the presence of valinomycin to generate the potential. The question of the net positive charge transfer accompanying the entry of each Ca2+ has not been settled; Rottenberg and Scarpa [30] have reported that the charge transfer is 2.…”

Section: Discussionmentioning

confidence: 99%

The Sodium‐Induced Efflux of Calcium from Heart Mitochondria

Crompton¹,

Capano²,

Carafoli³

1976

European Journal of Biochemistry

364

133

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The interrelations between the transport of Na+ and Ca2+ in heart mitochondria have been investigated. Na' induces a partial release of Ca2' from heart mitochondria; in the presence of ruthenium red the release of Ca2+ by Na' is complete. The rate of Caz+ release appears to be a function of [Nail3 and is stimulated by energy-linked respiration. Ca2' efflux is also induced by Li' although Na' is the preferred cation. The data are consistent with the existence of a system able to catalyze an exchange between Na' (or Lit) and Ca2+ across the inner membrane of heart mitochondria.The ability of mitochondria to accumulate Ca2+ by an energy-dependent process and, in so doing, to reduce the extramitochondrial Ca2+ concentration to the pM range is extensively documented (for reviews, see [1,2]). The influx of Ca2+ into heart mitochondria is strongly inhibited by physiological concentrations of Mg2+ [ 2 , 3 ] . However, an evaluation of the true of mitochondria in regulating the intracellular Ca2+ requires knowledge not only of how influx may be limited, but also of the process(es) by which Ca2+ is released from mitochondria. The observation [4] that Na' causes a release of the endogenous Ca2+ of isolated heart mitochondria is clearly relevant to this problem since heart is known to undergo small, but definite, variations in intracellular Na+ . This report is concerned with the interrelations between the transport of Ca2' and Na' in heart mitochondria, and presents evidence that these mitochondria contain a system able to catalyse an exchange between N a + and Ca2' across the inner membrane. MATERIALS AND METHODS Mitochondria1 PrepurationHeart mitochondria were isolated from female Sprague-Dawley rats using a Polytron homogenizer by the procedure described by Scarpa and Graziotti [5]. The medium used for homogenisation contained 210 mM mannitol, 70 mM sucrose, 10 mM Tris-HC1 pH 7.4, and 0.1 mM EDTA. The mitochondria were washed subsequently twice in the medium without EDTA. The mitochondria were suspended finally in medium without EDTA (approx. 20 mg of mitochondrial protein/ml).Rat liver mitochondria were prepared according to the procedure of Klingenberg and Slenczka [6] using media identical to those described for the preparation of heart mitochondria.The protein content of the mitochondria was determined by a modification of the biuret procedure [7] with bovine plasma albumen (Sigma Chemical Co.) as standard.Heart mitochondria were depleted of their endogenous Ca2+ by washing them in the presence of an inhibitor of respiration. Mitochondria containing about 50 mg of protein, were incubated at 25 "C in 10 ml of medium containing 120 mM KCl, 10 mM potassium (N-2-hydroxyethylpiperazine-N '-2-ethanesulphonic acid pH 7.2 and 30 pg of rotenone for 7 min. The suspension was diluted with 90 ml of ice-cold medium containing 210 mM mannitol and 70 mM sucrose and the mitochondria sedimented by centrifugation. The mitochondria were washed once more in the same manner. Mitochondria depleted in this way and incubated in the mediu...

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Section: Discussionmentioning

confidence: 99%

The Sodium‐Induced Efflux of Calcium from Heart Mitochondria

Crompton¹,

Capano²,

Carafoli³

1976

European Journal of Biochemistry

364

133

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“…inside-negative membrane potential (A$) constitutes the driving force for Ca2+ influx on a native Ca2+ carrier, denoted as the Ca2" uniporter [2,3].…”

Section: Introductionmentioning

confidence: 99%

A membrane potential‐modulated pathway for Ca²⁺ efflux in rat liver mitochondria

Bernardi¹,

Azzone²

1982

FEBS Letters

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“…Net Ca2 + accumulation by mitochondria is inhibited by very low concentrations of ruthenium red [3] which, at these concentrations, does not interfere with mitochondrial energy transduction [4,5] ; ruthenium red, therefore, is thought to inhibit by interacting with the system responsible for Ca2 + translocation across the inner membrane. The accumulation of Ca2+ by respiring mitochondria is generally considered to result from the electrical potential difference across the inner membrane (negative inside; [6]) and the passive influx of Ca2 + down its electrochemical gradient [5,7,8]. The ruthenium-red-sensitive system, therefore, probably catalyses an electrophoretic movement of Ca" across the inner membrane, although the magnitude of the net positive charge transfer per entry of each Ca2+ is not established [7,9].…”

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confidence: 99%

The Calcium‐Induced and Sodium‐Induced Effluxes of Calcium from Heart Mitochondria

Crompton¹,

Künzi²,

Carafoli³

1977

European Journal of Biochemistry

263

131

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Addition of Na', Li', Ca2+ or S?' induces efflux of the intramitochondrial 45Ca2+ from rat heart mitochondria. These reactions are inhibited by La3+ but not by ruthenium red. The ability of La3+ to inhibit has been exploited to develop an inhibitor-stop technique to study the effluxes of 45Ca2+ induced by Ca2+ and other cations. The Ca2+-induced efflux of 45Ca2' shows MichaelisMenten kinetics (Km, 13 pM) and is attributable to a Ca2+-Ca2+ exchange across the inner mitochondrial membrane with a stoichiometry of 1 : 1. The Ca2'-Ca2+ exchange and the Na+-induced efflux of Ca2+ show similar sensitivities to inhibition by La3+. Moreover, the Ca2+-Ca2+ exchange is inhibited by Na'. The Na+-dependent efflux of Ca" is stimulated by mitochondrial energisation without changing the affinity of the system for Na+ or Ca2+. In contrast, the Ca2+-Ca2' exchange is not influenced by the mitochondrial energy state. The data agree with the existence of an exchange-diffusion carrier in the inner membrane able to catalyse an exchange between intramitochondrial Ca2' and extramitochondrial Ca2+, Sr2+, Na' and Li+ . The energydependence of the exchanges is discussed.

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Calcium transport in mitochondria

Cited by 141 publications

References 14 publications

The Sodium‐Induced Efflux of Calcium from Heart Mitochondria

The Sodium‐Induced Efflux of Calcium from Heart Mitochondria

A membrane potential‐modulated pathway for Ca²⁺ efflux in rat liver mitochondria

The Calcium‐Induced and Sodium‐Induced Effluxes of Calcium from Heart Mitochondria

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Calcium transport in mitochondria

Cited by 141 publications

References 14 publications

The Sodium‐Induced Efflux of Calcium from Heart Mitochondria

The Sodium‐Induced Efflux of Calcium from Heart Mitochondria

A membrane potential‐modulated pathway for Ca2+ efflux in rat liver mitochondria

The Calcium‐Induced and Sodium‐Induced Effluxes of Calcium from Heart Mitochondria

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A membrane potential‐modulated pathway for Ca²⁺ efflux in rat liver mitochondria