Matrix free magnesium changes with metabolic state in isolated heart mitochondria

Biochemistry ◽  
1990 ◽  
Vol 29 (17) ◽  
pp. 4121-4128 ◽  
Author(s):  
Dennis W. Jung ◽  
Lynn Apel ◽  
Gerald P. Brierley
Keyword(s):  
Isolated Heart ◽  
Heart Mitochondria ◽  
Metabolic State ◽  
Matrix Free ◽  
Free Magnesium

scholarly journals A heart mitochondrial Ca2+-dependent pore of possible relevance to re-perfusion-induced injury. Evidence that ADP facilitates pore interconversion between the closed and open states

1990 ◽  
Vol 266 (1) ◽  
pp. 33-39 ◽  
Author(s):  
M Crompton ◽  
A Costi
Keyword(s):  
Arsenazo Iii ◽  
Heart Mitochondria ◽  
Ionophore A23187 ◽  
Relative Permeabilities ◽  
Pulsed Flow ◽  
Pore Closure ◽  
Open States ◽  
Matrix Free ◽  
Pore Number

The permeability properties of a putative Ca2(+)-activated pore in heart mitochondria, of possible relevance to re-perfusion-induced injury, have been investigated by a pulsed-flow solute-entrapment technique. The relative permeabilities of [14C]mannitol, [14C]sucrose and arsenazo III are consistent with permeation via a pore of about 2.3 nm diameter. Ca2+ removal with EGTA induced pore closure, and the mitochondria became ‘resealed’. The permeability of the unresealed mitochondria during resealing was markedly stimulated by 200 microM-ADP, and the relative permeabilities to solutes of different size were stimulated equally, indicating an increase in open-pore number, rather than an increase in pore dimensions. This is paradoxical, since ADP also stimulated the rate of resealing. The rate of EGTA-induced resealing was also stimulated by the Ca2+ ionophore A23187, which indicates that the rate of removal of matrix free Ca2+ is limiting for pore closure. An explanation for the paradox is suggested in which ADP facilitates pore interconversion between the closed and open states in permeabilized mitochondria, and pore closure in Ca2(+)-free mitochondria occurs much faster than previously thought.

On-line monitoring of the Krebs cycle in isolated heart mitochondria by13C NMR spectroscopy

1992 ◽  
Vol 30 (4) ◽  
pp. 347-358 ◽  
Author(s):  
Werner Offermann ◽  
Evi Fiedler ◽  
Corinna Helmle-Kolb ◽  
Werner Hofer ◽  
Harald Kugel ◽  
...  
Keyword(s):  
Nmr Spectroscopy ◽  
Isolated Heart ◽  
Krebs Cycle ◽  
Heart Mitochondria ◽  
On Line

Low rates of hydrogen peroxide production by isolated heart mitochondria associate with long maximum lifespan in vertebrate homeotherms

Aging Cell ◽  
2007 ◽  
Vol 6 (5) ◽  
pp. 607-618 ◽  
Author(s):  
Adrian J. Lambert ◽  
Helen M. Boysen ◽  
Julie A. Buckingham ◽  
Ting Yang ◽  
Andrej Podlutsky ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Isolated Heart ◽  
Heart Mitochondria ◽  
Maximum Lifespan ◽  
Hydrogen Peroxide Production

Effect of Adriamycin on superoxide radical generation in isolated heart mitochondria

BIOPHYSICS ◽  
2007 ◽  
Vol 52 (6) ◽  
pp. 582-586 ◽  
Author(s):  
I. V. Sviryaeva ◽  
E. K. Ruuge ◽  
K. B. Shumaev
Keyword(s):  
Superoxide Radical ◽  
Isolated Heart ◽  
Heart Mitochondria ◽  
Radical Generation

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Drug Research ◽  
2020 ◽  
Vol 70 (04) ◽  
pp. 151-157 ◽  
Author(s):  
Enayatollah Seydi ◽  
Yasaman Tabbati ◽  
Jalal Pourahmad
Keyword(s):  
Mitochondrial Membrane ◽  
Heart Diseases ◽  
Isolated Heart ◽  
Chain Complex ◽  
Heart Mitochondria ◽  
Cytochrome C Release ◽  
Drug Induced ◽  
Rat Heart Mitochondria ◽  
Β Receptor ◽  
Underlying Mechanisms

AbstractPropranolol and atenolol are known as β receptor blocker drugs. These drugs are used to treat some heart diseases. There are controversies in the relationship between the use of beta-blocker drugs and the level of reactive oxygen species (ROS). Mitochondria as one of the most important sources of ROS are considered as one of the targets of drug-induced cardiotoxicity. The aim of this study was to evaluate the effects of propranolol and atenolol on mitochondria isolated from the heart. To achieve this aim, several markers of mitochondrial and cellular toxicity were evaluated. The key results of this study are the increased ROS level, collapse in mitochondrial membrane potential (MMP), mitochondrial swelling and cytochrome c release as well as disruption of respiratory chain complex II in mitochondria in isolated heart mitochondria after exposure to propranolol and atenolol. The results indicate an increase in caspase-3 activity and a decrease in the ATP level in cardiomyocytes after exposure to propranolol and atenolol. The underlying mechanisms of propranolol and atenolol induced cardiotoxicity may be associated with alterations in mitochondrial function, oxidative stress, and changes in the mitochondrial membrane.

Activation of energy-linked K+ accumulation in isolated heart mitochondria by non-ionic detergents

1971 ◽  
Vol 43 (1) ◽  
pp. 50-57 ◽  
Author(s):  
G.P. Brierley ◽  
M. Jurkowitz ◽  
K.M. Scott ◽  
K.M. Hwang ◽  
A.J. Merola
Keyword(s):  
Isolated Heart ◽  
Heart Mitochondria ◽  
Ionic Detergents

Estimation of matrix pH in isolated heart mitochondria using a fluorescent probe

1989 ◽  
Vol 178 (2) ◽  
pp. 348-354 ◽  
Author(s):  
Dennis W. Jung ◽  
Michael H. Davis ◽  
Gerald P. Brierley
Keyword(s):  
Fluorescent Probe ◽  
Isolated Heart ◽  
Heart Mitochondria

scholarly journals Proportion of active dephosphorylated pyruvate dehydrogenase complex in heart and isolated heart mitochondria is decreased in obese hyperinsulinaemic mice

1984 ◽  
Vol 217 (1) ◽  
pp. 117-121 ◽  
Author(s):  
A L Kerbey ◽  
I D Caterson ◽  
P F Williams ◽  
J R Turtle
Keyword(s):  
Insulin Resistance ◽  
Enzyme Activity ◽  
Pyruvate Dehydrogenase ◽  
Glucose Oxidation ◽  
Isolated Heart ◽  
Pyruvate Dehydrogenase Complex ◽  
Heart Mitochondria ◽  
Mouse Heart ◽  
Inhibitory Effects ◽  
Dehydrogenase Complex

The proportion of active, dephosphorylated, pyruvate dehydrogenase complex was decreased in the mouse heart by obesity (by 56%), and this decrease in enzyme activity persisted during preparation and extraction of heart mitochondria. Phosphorylation and inactivation of pyruvate dehydrogenase may be a major factor in mediating the inhibitory effects of obesity on glucose oxidation in muscle, and this may represent an important mechanism in the development and/or expression of cellular insulin-resistance.

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