Role of mitochondria in control of calcium content of liver slices

Rossum, G.D.V. Van; Smith, Kathleen; Beeton, Phyllis

doi:10.1038/260335a0

Cited by 37 publications

(13 citation statements)

References 16 publications

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“…(2) The inclusion of I mM I.a3+in the homogenization buffer may act to precipitate some non-mitochondrial protein [7], and this precipitated protein may be carried along with the isolated mitochondria, hence, the calcium content~mg protein may be higher than that reported here. Measurements of calcium changes in other cell organelles or membranes will be required to determine whether or not these structures are involved in the mobilization of intracellular calcium by a-agonists or other hormones.…”

Section: Resultsmentioning

confidence: 64%

α‐adrenergic mobilization of hepatic mitochondrial calcium

et al. 1979

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Section: Resultsmentioning

confidence: 64%

α‐adrenergic mobilization of hepatic mitochondrial calcium

et al. 1979

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“…In many instances, the enzymes that are sensitive to calcium are also affected by magnesium, with the two ions exhibiting antagonistic effects on such enzymes (1, 50 55). Since mitochondria are known to be able to act as efficient calcium buffers that regulate extra-mitochondrial free calcium concentrations (50,56) and thus alter cytosolic Mg2+/Ca 2+ ratios (1), it was of interest to see how calcium uptake by control and glucagontreated mitochondria would be affected by the presence or absence of Mg 2+ in the incubation medium. There have been conflicting reports in the literature concerning the effect of Mg 2+.…”

Section: -mentioning

confidence: 99%

The effect of glucagon on the kinetics of hepatic mitochondrial calcium uptake

1981

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Previous work by this and other laboratories has shown that glucagon administration stimulates calcium uptake by subsequently isolated hepatic mitochondria. This stimulation of hepatic mitochondrial Ca2+ uptake by in vivo administration of glucagon was further characterized in the present report. Maximal stimulation of mitochondrial Ca2+ accumulation was achieved between 6-10 min after the intravenous injection of glucagon into intact rats. Under control conditions, Ca2+ uptake was inhibited by the presence of Mg2+ in the incubation medium. Glucagon treatment, however, appeared to obliterate the observed inhibition by Mg2+ of mitochondrial Ca2+ uptake. Kinetic experiments revealed the usual sigmoidicity associated with initial velocity curves for mitochondrial calcium uptake. Glucagon treatment did not alter this sigmoidal relationship. Glucagon treatment significantly increased the V max for Ca2+ uptake from 292 +/- 22 to 377 +/- 34 nmoles Ca2+/min per mg protein (n = 8) but did not affect the K 0.5, (6.5-8.6 microM). Since the major kinetic change in mitochondrial Ca2+ uptake evoked by glucagon is an increase in V max, the enhancement mechanism is likely to be an increase either in the number of active transport sites available to Ca2+ or in the rate of Ca2+ carrier movement across the mitochondrial membranes.

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“…This difference may be attributed to an uptake of "iCa originating from other cellular pools during the homogenization in the absence of chelators (Van Rossum et al 1976). According to this view, Ca chelators or transport inhibitors prevent "Ca uptake by mitochondria during the 10 see homogenization.…”

Section: Electrolyte Determinationmentioning

confidence: 99%

Fluxes and distribution of calcium in rat liver cells: kinetic analysis and identification of pools

Claret-Berthon¹,

Claret²,

Mazet³

1977

The Journal of Physiology

100

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4. Extracellular Ca pools were studied using competitor of Ca binding (La) or Ca chelators (EGTA). La displaced specifically a homogeneous pool of Ca (r = 5-1 min) which represented a fraction (55 Emole . kg-') of the rapidly exchangeable Ca (first compartment) without perturbing other external pools. On the other hand, EGTA displaced completely that compartment, and about 85 % of the Ca of the third compartment. These results suggest that the first and the major fraction of the third compartments are extracellular. They account for 63 % of total exchangeable Ca. 5. A model of distribution and exchange of Ca in hepatocytes is proposed.* Attache INSERM.

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Role of mitochondria in control of calcium content of liver slices

Cited by 37 publications

References 16 publications

α‐adrenergic mobilization of hepatic mitochondrial calcium

α‐adrenergic mobilization of hepatic mitochondrial calcium

The effect of glucagon on the kinetics of hepatic mitochondrial calcium uptake

Fluxes and distribution of calcium in rat liver cells: kinetic analysis and identification of pools

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