Ion transport by heart mitochondria

Scott, K.M.; Hwang, Ki Won; Jurkowitz, Marianne S.; Brierley, Gerald P.

doi:10.1016/0003-9861(71)90413-9

Cited by 60 publications

(5 citation statements)

References 23 publications

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“…We are loth to ascribe the second effect to increased competition for available energy between Ca2+ and K+ transport, since this would require the precedence of K+ transport in the use of respiratory energy. The lack of respiratory stimulation by Pb2+ in KCl and the similar effects of Pb2+ on Ca2+ removal in KCI and sucrose media all suggest that the swelling observed by Scott et al (1971) was another symptom of the inhibition of the production or use of respiratory energy by Pb2+.…”

Section: Discussionmentioning

confidence: 88%

“…We do not believe the second effect is due to inhibition of pyruvate uptake or oxidation since, although both were subject to inhibition by Pb2+, neither was decreased by more than 50%, even with 10nmol of Pb2+/mg of protein. Scott et al (1971) deduced from swelling studies that Pb2+ increases mitochondrial Vol. 158 K+ permeability.…”

Section: Discussionmentioning

confidence: 99%

“…It is established both in vivo and in vitro that mitochondria are one of the major subcellular loci of Pb2+ accumulation (e.g. Scott et al, 1971;Murakami & Hirosawa, 1973;Ophus & Gulvag, 1974;Asokan, 1974;Moore et al, 1975). A nuclear protein that binds Pb2+ forming inclusion bodies may fulfill a detoxifying role in the kidney, preventing the action ofPb2+ on mitochondria (Goyer, 1971).…”

Section: Discussionmentioning

confidence: 99%

“…Now we report that one-tenth of that Pb2+ concentration significantly decreases the rate, and hence the extent, of Ca2+ removal by energized heart mitochondria in the absence of P1. The only previous report is that of Scott et al (1971) who comment briefly that Pb2+ competes with Ca2+ for uptake into de-energized mitochondria.…”

mentioning

confidence: 99%

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The effect of lead on the calcium-handling capacity of rat heart mitochondria

Parr¹,

Harris²

1976

Biochemical Journal

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1. Very low concentrations of Pb2+ decrease the capacity of rat heart mitochondria, oxidizing pyruvate plus malate, to remove Ca2+ from the medium. 2. The primary effect is on the rate of Ca2+ sequestration; this is reflected in the overall extent of Ca2+ removal. 3. Pb2+ has at least two separate actions. Below about 0.5 nmol/mg of protein, it acts solely by competing with Ca2+ (Ki = 0.4 muM); above this concentration it also inhibits the production or use of respiratory energy, so that at 1 nmol of Pb2+/mg of protein, Ca2+ removal is almost completely abolished. 4. Pb2+ inhibits coupled and uncoupled respiratory O2 use by mitochondria oxidizing pyruvate plus malate, but at higher concentrations than those that affect Ca2+ removal; similar concentrations of Pb2+ inhibit pyruvate uptake, but not malate uptake, by the mitochondria. 5. Mg2+ only decreases Ca2+ removal by competition, and is a far-less effective competitor than Pb2+ (Ki = 0.15 mM). It is possible that the primary cause of the second effect of Pb2+ is displacement of membrane Mg2+. 6. The consequences of these results are discussed in terms of the possible involvement of heart mitochondria in excitation-contraction coupling, and the Pb2+ levels that might occur in heart tissue in vivo.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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The effect of lead on the calcium-handling capacity of rat heart mitochondria

Parr¹,

Harris²

1976

Biochemical Journal

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“…RR prevented the Pb 2+ -induced ∆Ψ mito decline, state 3 respiration decrease, and Ca 2+ release in RKM energized by succinate but not by NAD-dependent substrates [60,61]. In experiments with bovine heart mitochondria (BHM), energized by CI-CII substrates, Pb 2+ inhibited Ca 2+ uptake; resulted in mitochondrial swelling and ∆Ψ mito decline; increased the inner mitochondrial membrane (IMM) passive K + permeability; and decreased K + uptake and mitochondrial respiration in 4, 3, 3U CCP , and 3U DNP states [64][65][66]. Some of these Pb 2+ effects were blocked by Pi or chlorpromazine [66].…”

Section: Tl(i)mentioning

confidence: 99%

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Korotkov

2023

IJMS

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This review analyzes the causes and consequences of apoptosis resulting from oxidative stress that occurs in mitochondria and cells exposed to the toxic effects of different-valence heavy metals (Ag+, Tl+, Hg2+, Cd2+, Pb2+, Al3+, Ga3+, In3+, As3+, Sb3+, Cr6+, and U6+). The problems of the relationship between the integration of these toxic metals into molecular mechanisms with the subsequent development of pathophysiological processes and the appearance of diseases caused by the accumulation of these metals in the body are also addressed in this review. Such apoptosis is characterized by a reduction in cell viability, the activation of caspase-3 and caspase-9, the expression of pro-apoptotic genes (Bax and Bcl-2), and the activation of protein kinases (ERK, JNK, p53, and p38) by mitogens. Moreover, the oxidative stress manifests as the mitochondrial permeability transition pore (MPTP) opening, mitochondrial swelling, an increase in the production of reactive oxygen species (ROS) and H2O2, lipid peroxidation, cytochrome c release, a decline in the inner mitochondrial membrane potential (ΔΨmito), a decrease in ATP synthesis, and reduced glutathione and oxygen consumption as well as cytoplasm and matrix calcium overload due to Ca2+ release from the endoplasmic reticulum (ER). The apoptosis and respiratory dysfunction induced by these metals are discussed regarding their interaction with cellular and mitochondrial thiol groups and Fe2+ metabolism disturbance. Similarities and differences in the toxic effects of Tl+ from those of other heavy metals under review are discussed. Similarities may be due to the increase in the cytoplasmic calcium concentration induced by Tl+ and these metals. One difference discussed is the failure to decrease Tl+ toxicity through metallothionein-dependent mechanisms. Another difference could be the decrease in reduced glutathione in the matrix due to the reversible oxidation of Tl+ to Tl3+ near the centers of ROS generation in the respiratory chain. The latter may explain why thallium toxicity to humans turned out to be higher than the toxicity of mercury, lead, cadmium, copper, and zinc.

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Role of anion exchange and thiol groups in the regulation of potassium efflux by lead in human erythrocytes

1996

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Pb2+ is thought to enter erythrocytes through anion exchange (AE) and to remain in the cell by binding to thiol groups. To define the role of AE mechanisms and thiol groups in Pb2+ toxicity, we studied the effects of drugs and conditions that modify AE and that modify thiol groups on the ability of Pb2+ to stimulate potassium efflux as measured with 86Rb. The most potent stimulation of 86Rb efflux by Pb2+ occurred when conditions were optimal for the AE mechanism--that is, when bicarbonate was included in the buffer or a buffer made with Nal or NaCl rather than NaClO4 or NaNO3 was used. Furthermore, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid and 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfuonic acid, potent inhibitors of the AE mechanism, completely inhibited stimulation of the 86Rb efflux by Pb2+. These conditions or inhibitors did not affect stimulation of the 86Rb efflux by ionomycin plus Ca2+. A role for Ca2+ channels was dismissed because the inorganic Ca2+ channel blockers, Cd2+ or Mn2+, did not prevent stimulation of 86Rb efflux by Pb2+ but did inhibit stimulation by ionomycin plus Ca2+. 86Rb efflux was more sensitive to Pb2+ if erythrocytes were treated for 15 min with thiol-modifying reagents that enter cells, such as iodoacetamide, N-ethylmaleimide, or dithiothreitol, than to reduced glutathione, a thiol-modifying reagent that is not permeable to the cell. Thus, in erythrocytes the AE mechanism and internal thiol groups are critical factors that affect the stimulation of a Ca(2+)-dependent process by Pb2+.

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Ion transport by heart mitochondria

Cited by 60 publications

References 23 publications

The effect of lead on the calcium-handling capacity of rat heart mitochondria

The effect of lead on the calcium-handling capacity of rat heart mitochondria

Mitochondrial Oxidative Stress Is the General Reason for Apoptosis Induced by Different-Valence Heavy Metals in Cells and Mitochondria

Role of anion exchange and thiol groups in the regulation of potassium efflux by lead in human erythrocytes

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