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

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.

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Protective effects of verapamil and diltiazem against inorganic phosphate induced impairment of oxidative phosphorylation of isolated heart mitochondria

Biochemical Pharmacology ◽

10.1016/0006-2952(81)90588-8 ◽

1981 ◽

Vol 30 (18) ◽

pp. 2603-2610 ◽

Cited By ~ 22

Author(s):

Pál L. Vághy ◽

Mohammed A. Matlib ◽

László Szekeres ◽

Arnold Schwartz

Keyword(s):

Oxidative Phosphorylation ◽

Inorganic Phosphate ◽

Isolated Heart ◽

Heart Mitochondria ◽

Protective Effects

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

Analytical Biochemistry ◽

10.1016/0003-2697(89)90651-9 ◽

1989 ◽

Vol 178 (2) ◽

pp. 348-354 ◽

Cited By ~ 46

Author(s):

Dennis W. Jung ◽

Michael H. Davis ◽

Gerald P. Brierley

Keyword(s):

Fluorescent Probe ◽

Isolated Heart ◽

Heart Mitochondria

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

Biochemical Journal ◽

10.1042/bj2170117 ◽

1984 ◽

Vol 217 (1) ◽

pp. 117-121 ◽

Cited By ~ 5

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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