Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Drug Toxicity: Dose-Dependent Reactions01:24

Drug Toxicity: Dose-Dependent Reactions

171
Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
171
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

19.6K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
19.6K
The Electron Transport Chain01:30

The Electron Transport Chain

21.5K
The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q...
21.5K
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

1.9K
Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
1.9K
Drug Toxicity: Risk factors01:24

Drug Toxicity: Risk factors

182
Adverse Drug Reactions (ADRs) are potential complications that arise during pharmacotherapy, influenced by multiple risk factors. Age plays a significant role; both neonates and the elderly are at heightened risk due to their respective immature and diminished metabolic and elimination processes. Gender also impacts ADRs, with females experiencing a 1.5 to 1.7-fold greater risk than males, which may be linked to pharmacokinetic, pharmacodynamic, and hormonal differences. Notably, neonates, the...
182
Drug toxicity: Drug–Drug Interaction01:30

Drug toxicity: Drug–Drug Interaction

341
Drug–drug interactions can precipitate toxicity through multiple mechanisms. Absorption interactions alter how drugs enter the body, exemplified when ranitidine increases the absorption of basic drugs, while cholestyramine decreases the levels of propranolol. Protein binding interactions occur when drugs share the same binding sites on plasma proteins. Drugs like aspirin and warfarin, when bound in excess, can lead to increased free drug concentrations, enhancing the potential for...
341

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Low-dose levosimendan infusions in advanced heart failure: efficacy, safety, and factors associated with outcomes.

Clinical research in cardiology : official journal of the German Cardiac Society·2026
Same author

Drug sequestration and metabolite formation: key pharmacokinetic challenges for levosimendan use during ECMO support in cardiogenic shock.

Journal of intensive care·2026
Same author

Cleavage and inactivation of poly(ADP-ribose) polymerase in peripheral blood mononuclear cells of patients with acute respiratory distress syndrome.

Respiratory research·2026
Same author

Impact of a clinical decision protocol on survival and neurological outcome following extracorporeal cardiopulmonary resuscitation.

Journal of intensive care·2026
Same author

Thermal Preconditioning During Ex-vivo Lung Perfusion for the Rehabilitation of Damaged Lung Grafts before Transplantation.

Journal of visualized experiments : JoVE·2025
Same author

Low-dose photodynamic therapy promotes vascular E-selectin expression in chest malignancies, improving immune infiltration and tumor control.

Journal for immunotherapy of cancer·2025

Related Experiment Video

Updated: Apr 3, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

15.4K

Drug-induced mitochondrial dysfunction and cardiotoxicity.

Zoltán V Varga1, Peter Ferdinandy2, Lucas Liaudet3

  • 1Laboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland; Cardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary;

American Journal of Physiology. Heart and Circulatory Physiology
|September 20, 2015
PubMed
Summary

Mitochondrial dysfunction from various drugs can cause heart damage. This review explores drug-induced cardiotoxicity mechanisms and cardioprotective strategies to prevent heart disease.

Keywords:
cardiomyopathydrug developmentheartheart failurereactive oxygen speciestoxicology

More Related Videos

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
07:03

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics

Published on: August 23, 2024

1.7K
Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

12.4K

Related Experiment Videos

Last Updated: Apr 3, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

15.4K
Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
07:03

Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics

Published on: August 23, 2024

1.7K
Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle
09:40

Phosphorus-31 Magnetic Resonance Spectroscopy: A Tool for Measuring In Vivo Mitochondrial Oxidative Phosphorylation Capacity in Human Skeletal Muscle

Published on: January 19, 2017

12.4K

Area of Science:

  • Cardiovascular Research
  • Mitochondrial Biology
  • Pharmacology

Background:

  • Mitochondria are vital for heart health; their dysfunction leads to cell death and cardiovascular issues.
  • Numerous drugs, including anticancer agents, antivirals, and antidiabetics, can harm cardiac mitochondria.
  • Illicit substances also contribute to mitochondria-related cardiotoxicity.

Purpose of the Study:

  • To review the mechanisms of drug-induced cardiotoxicity targeting mitochondria.
  • To discuss potential strategies for preventing or mitigating this toxicity.

Main Methods:

  • Literature review of studies on drug mechanisms and cardiotoxicity.
  • Analysis of pathways involved in mitochondrial dysfunction.
  • Identification of cardioprotective approaches.

Main Results:

  • Drug-induced cardiotoxicity involves interference with mitochondrial respiration and enzymes.
  • Mechanisms include uncoupling, inhibition of oxidative phosphorylation, and increased oxidative stress.
  • Cardiotoxicity can manifest acutely or after prolonged exposure, complicating diagnosis.

Conclusions:

  • Understanding mitochondria-mediated cardiotoxicity is crucial for safe drug use.
  • Developing cardioprotective strategies is essential to prevent drug-induced heart damage.
  • Further research is needed to identify effective preventive measures.