Drug induced mitochondrial dysfunction: Mechanisms and adverse clinical consequences

Area of Science:

• Biochemistry
• Pharmacology
• Toxicology

Background:

• Mitochondria are vital for cellular energy and metabolism.
• Numerous medications can disrupt normal mitochondrial function.
• This disruption can lead to significant adverse health effects.

Purpose of the Study:

• To review medications that impair mitochondrial function.
• To elucidate the mechanisms behind drug-induced mitochondrial dysfunction.
• To outline the clinical consequences of these interactions.

Main Methods:

• Literature review of experimental and clinical studies.
• Analysis of drug classes affecting mitochondria.
• Correlation of mitochondrial effects with clinical outcomes.

Main Results:

• Common drugs can cause mitochondrial dysfunction via various mechanisms (ROS production, altered permeability, impaired respiration, mtDNA damage, inhibited beta-oxidation).
• Clinical manifestations include hepatotoxicity, enteropathy, myelosuppression, lipodystrophy, and neuropsychiatric effects.
• The specific drug and its mitochondrial target determine the toxicity.

Conclusions:

• Drug-mitochondrial interactions are a significant cause of adverse drug reactions.
• Awareness of these interactions aids clinicians in predicting and preventing toxicity.
• Knowledge facilitates safer drug prescribing and regimen adjustments.