Title:The Role of Therapeutic Drugs on Acquired Mitochondrial Toxicity
VOLUME: 17 ISSUE: 7
Author(s):Constanza Morén, Diana Luz Juárez-Flores, Francesc Cardellach and Glòria Garrabou
Affiliation:Muscle Research and Mitochondrial Function Laboratory, Muscle Research Unit, Cellex-IDIBAPSFaculty of Medicine, University of Barcelona, Internal Medicine Department- Hospital Clínic of Barcelona (Barcelona, Spain) and U722-CIBERER (ISCIII, Madrid, Spain).
Keywords:Adverse effects, medication, mitochondria, mitotoxicity, secondary mitochondriopathies, toxicity.
Abstract:Background: Certain therapeutic drugs used in medical practice may trigger mitochondrial
toxicity leading to a wide range of clinical symptoms including deafness, neuropathy,
myopathy, hyperlactatemia, lactic acidosis, pancreatitis and lipodystrophy, among others, which
could even compromise the life of the patient.
Objectives: The aim of this work is to review the potential mitochondrial toxicity derived from
drugs used in health care, including anesthetics, antiepileptics, neuroleptics, antidepressants,
antivirals, antibiotics, antifungals, antimalarics, antineoplastics, antidiabetics, hypolipemiants,
antiarrhythmics, anti-inflammatories and nitric oxide.
Methods: We herein have reviewed data from experimental and clinical studies to document the
molecular mitochondrial basis, potential biomarkers and putative clinical symptoms associated to
secondary effects of drugs.
Results: One hundred and forty-five articles were selected and the information was organized by
means of the primary target to which pharmacologic drugs were directed. Adverse toxic events were classified depending
on the mitochondrial offtarget effect and whether they had been demonstrated in the experimental or clinical setting.
Conclusions: Since treatment of acquired mitochondriopathies remains supportive and therapeutic interventions cannot
be avoided, information of molecular and clinical consequences of toxic exposure becomes fundamental to assess riskbenefit
imbalance of treatment prescription. Additionally, there is a crucial need to develop less mitochondrial toxic
compounds, novel biomarkers to follow up mitochondrial toxicity (or implement those already proposed) and new
approaches to prevent or revert unintended mitochondrial damage.
