Pathogenesis of Amiodarone-Related Toxicity

Abstract
Amiodarone is an antiarrhythmic drug widely used to treat atrial and ventricular arrhythmias. On the other hand, amiodarone can cause toxicity in many organs such as the heart, lungs, gastrointestinal tract, liver, eyes, thyroid, and skin during and after treatment. The tendency of amiodarone to accumulate in organs with a high lipid content increases its half-life and causes prolonged therapeutic and toxic effects. Oxidative stress is thought to be the main factor in amiodarone-induced tissue damage. Amiodarone has been shown to cause oxidative damage through an increase in reactive oxygen species (ROS) and a decrease in aioxidants. Amiodarone also disrupts the mitochondrial respiratory chain and decreases adenosine triphosphate (ATP) levels, which are among the causes of toxicity. Amiodarone has also been shown to increase levels of pro-inflammatory cytokines. The increase in these cytokines may further increase ROS levels and exacerbate the damage. On the other hand, the structural feature of amiodarone has been considered another cause of toxicity, and thyroid damage has been attributed to its similarity to thyroxine and iodine content. Considering the widespread use of amiodarone, toxic effects and prevention of toxicity become more important. Given the significant role of oxidative stress and inflammation in amiodarone-related toxic effects, antioxidant and anti-inflammatory therapies are emerging as promising strategies to mitigate these adverse effects. In addition, studies to maintain cellular ATP levels at physiological levels may emerge as an important treatment strategy to prevent amiodarone toxicity.

Cite this article as: Bulut S, Aksakal E, Süleyman H. Pathogenesis of amiodarone-related toxicity. Arch Basic Clin Res. 2025;7(1):68-70.