Drug Res (Stuttg) 2020; 70(04): 151-157
DOI: 10.1055/a-1112-7032
Original Article
© Georg Thieme Verlag KG Stuttgart · New York

Toxicity of Atenolol and Propranolol on Rat Heart Mitochondria

Enayatollah Seydi
1  Department of Occupational Health and Safety Engineering, School of Health, Alborz University of Medical Sciences, Karaj, Iran
2  Research Center for Health, Safety and Environment, Alborz University of Medical Sciences, Karaj, Iran
,
Yasaman Tabbati
3  Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
,
Jalal Pourahmad
3  Department of Pharmacology and Toxicology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
› Author Affiliations
Further Information

Publication History

received 20 December 2019

accepted 27 January 2020

Publication Date:
02 March 2020 (online)

Abstract

Propranolol 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.