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Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Enayatollah Seydi1,2, Yasaman Tabbati3, Jalal Pourahmad3

  • 1Department of Occupational Health and Safety Engineering, School of Health, Alborz University of Medical Sciences, Karaj, Iran.

Drug Research
|March 3, 2020
PubMed

Insights

Beta-blockers like propranolol and atenolol may harm heart mitochondria by increasing reactive oxygen species (ROS) and impairing function. This study reveals potential cardiotoxicity mechanisms linked to oxidative stress and mitochondrial damage.

Area of Science:

  • Cardiovascular Pharmacology
  • Mitochondrial Toxicology
  • Biochemistry

Background:

  • Beta-blockers, including propranolol and atenolol, are widely used for cardiac conditions.
  • Controversies exist regarding the impact of beta-blockers on reactive oxygen species (ROS) production.
  • Mitochondria are key sources of ROS and potential targets for drug-induced cardiotoxicity.

Purpose of the Study:

  • To investigate the effects of propranolol and atenolol on isolated heart mitochondria.
  • To evaluate specific markers of mitochondrial and cellular toxicity induced by these beta-blockers.

Main Methods:

  • Isolation of mitochondria from heart tissue.
  • Assessment of mitochondrial membrane potential (MMP).
  • Measurement of ROS levels, mitochondrial swelling, and cytochrome c release.
  • Evaluation of respiratory chain complex II activity.
  • Analysis of caspase-3 activity and ATP levels in cardiomyocytes.

Main Results:

  • Propranolol and atenolol exposure led to increased ROS levels in isolated heart mitochondria.
  • A significant collapse in MMP, mitochondrial swelling, and cytochrome c release were observed.
  • Disruption of respiratory chain complex II activity was evident.
  • Cardiomyocytes showed increased caspase-3 activity and decreased ATP levels.

Conclusions:

  • Propranolol and atenolol can induce cardiotoxicity through mechanisms involving mitochondrial dysfunction.
  • Oxidative stress and alterations in mitochondrial membrane integrity are implicated in this toxicity.
  • These findings highlight potential risks associated with beta-blocker use and warrant further investigation.

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