Contribution of the mitochondrial permeability transition to lethal injury after exposure of hepatocytes to t-butylhydroperoxide (Q36700328)

8 November 2017

Contribution of the mitochondrial permeability transition to lethal injury after exposure of hepatocytes to t-butylhydroperoxide (English)

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8 November 2017

A L Nieminen

1

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8 November 2017

A K Saylor

2

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8 November 2017

S A Tesfai

3

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8 November 2017

B Herman

4

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8 November 2017

J J Lemasters

5

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8 November 2017

language of work or name

English

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publication date

1 April 1995

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8 November 2017

8

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inferred from page(s)

published in

Biochemical Journal

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8 November 2017

307 ( Pt 1)

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8 November 2017

99-106

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Mitochondrial and glycolytic dysfunction in lethal injury to hepatocytes by t-butylhydroperoxide: protection by fructose, cyclosporin A and trifluoperazine.

8 November 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore. I. Evidence for two separate Me2+ binding sites with opposing effects on the pore open probability.

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Cyclosporin and carnitine prevent the anoxic death of cultured hepatocytes by inhibiting the mitochondrial permeability transition.

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Recruitment of mitochondrial cyclophilin to the mitochondrial inner membrane under conditions of oxidative stress that enhance the opening of a calcium-sensitive non-specific channel

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

The voltage sensor of the mitochondrial permeability transition pore is tuned by the oxidation-reduction state of vicinal thiols. Increase of the gating potential by oxidants and its reversal by reducing agents.

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

A quantitative stereological description of the ultrastructure of normal rat liver parenchymal cells

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Chemiosmotic coupling in oxidative and photosynthetic phosphorylation

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Fructose prevents hypoxic cell death in liver

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Membrane potential can be determined in individual cells from the nernstian distribution of cationic dyes

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Irreversible injury in anoxic hepatocytes precipitated by an abrupt increase in plasma membrane permeability

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Inhibition by cyclosporin A of a Ca2+-dependent pore in heart mitochondria activated by inorganic phosphate and oxidative stress

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Protection by acidotic pH and fructose against lethal injury to rat hepatocytes from mitochondrial inhibitors, ionophores and oxidant chemicals.

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Mechanisms by which mitochondria transport calcium

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Protection by acidotic pH against anoxic cell killing in perfused rat liver: evidence for a pH paradox.

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Phenylarsine oxide induces the cyclosporin A-sensitive membrane permeability transition in rat liver mitochondria

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

The giant channel of the inner mitochondrial membrane is inhibited by cyclosporin A.

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Calcium-dependent opening of a non-specific pore in the mitochondrial inner membrane is inhibited at pH values below 7. Implications for the protective effect of low pH against chemical and hypoxic cell damage

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

The mitochondrial megachannel is the permeability transition pore

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Modulation of the mitochondrial cyclosporin A-sensitive permeability transition pore by the proton electrochemical gradient. Evidence that the pore can be opened by membrane depolarization

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Prooxidant-induced Ca2+ release from liver mitochondria. Specific versus nonspecific pathways

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

Protection by Cyclosporin A of ischemia/reperfusion-induced damage in isolated rat hearts.

28 June 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1136750

The equivalent pore radius of intact and damaged mitochondria and the mechanism of active shrinkage

5 September 2018

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12 December 2020

Action of cyclosporine on mitochondrial calcium fluxes

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12 December 2020

Kinetic evidence for a heart mitochondrial pore activated by Ca2+, inorganic phosphate and oxidative stress. A potential mechanism for mitochondrial dysfunction during cellular Ca2+ overload

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12 December 2020

Cyclosporin A is a potent inhibitor of the inner membrane permeability transition in liver mitochondria

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12 December 2020

Swelling, reductive stress, and cell death during chemical hypoxia in hepatocytes

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12 December 2020

Cyclosporin A-sensitive and insensitive mechanisms produce the permeability transition in mitochondria

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12 December 2020

N-acetyl-p-benzoquinone imine induces Ca2+ release from mitochondria by stimulating pyridine nucleotide hydrolysis

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12 December 2020

Modulation of the mitochondrial permeability transition pore. Effect of protons and divalent cations

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12 December 2020

Cyclosporin A protects hepatocytes subjected to high Ca2+ and oxidative stress

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12 December 2020

Synergism of cyclosporin A and phospholipase inhibitors in protection against lethal injury to rat hepatocytes from oxidant chemicals

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12 December 2020

Intracellular pH and Ca2+ homeostasis in the pH paradox of reperfusion injury to neonatal rat cardiac myocytes

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12 December 2020

ATP depletion rather than mitochondrial depolarization mediates hepatocyte killing after metabolic inhibition

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12 December 2020

Effects of phospholipase A2 inhibitors on ruthenium red-induced Ca2+ release from mitochondria

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12 December 2020

Identifiers

DOI

10.1042/BJ3070099

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8 November 2017

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8 November 2017

PubMed publication ID

7718000

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