Drug induced mitochondrial dysfunction

Mechanisms and adverse clinical consequences

Madhusudanarao Vuda, Ashwin Kamath

Research output: Contribution to journalReview article

11 Citations (Scopus)

Abstract

Several commonly used medications impair mitochondrial function resulting in adverse effects or toxicities. Drug induced mitochondrial dysfunction may be a consequence of increased production of reactive oxygen species, altered mitochondrial permeability transition, impaired mitochondrial respiration, mitochondrial DNA damage or inhibition of beta-oxidation of fatty acids. The clinical manifestation depends on the specific drug and its effect on mitochondria. Given the ubiquitous presence of mitochondria and its central role in cellular metabolism, drug-mitochondrial interactions may manifest clinically as hepatotoxicity, enteropathy, myelosuppression, lipodystrophy syndrome or neuropsychiatric adverse effects, to name a few. The current review focuses on specific drug groups which adversely affect mitochondria, the mechanisms involved and the clinical consequences based on the data available from experimental and clinical studies. Knowledge of these adverse drug-mitochondrial interactions may help the clinicians foresee potential issues in individual patients, prevent adverse drug reactions or alter drug regimens to enhance patient safety.

Original languageEnglish
Pages (from-to)63-74
Number of pages12
JournalMitochondrion
Volume31
DOIs
Publication statusPublished - 01-11-2016

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Mitochondria
Drug Interactions
Pharmaceutical Preparations
Lipodystrophy
Patient Safety
Drug-Related Side Effects and Adverse Reactions
Mitochondrial DNA
DNA Damage
Names
Permeability
Reactive Oxygen Species
Respiration
Fatty Acids
Clinical Studies

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Molecular Biology
  • Cell Biology

Cite this

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Drug induced mitochondrial dysfunction : Mechanisms and adverse clinical consequences. / Vuda, Madhusudanarao; Kamath, Ashwin.

In: Mitochondrion, Vol. 31, 01.11.2016, p. 63-74.

Research output: Contribution to journalReview article

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