UNIT 2.15 Current Concepts in Drug-Induced Mitochondrial Toxicity

  1. Sashi Nadanaciva,
  2. Yvonne Will

Published Online: 1 MAY 2009

DOI: 10.1002/0471140856.tx0215s40

Current Protocols in Toxicology

Current Protocols in Toxicology

How to Cite

Nadanaciva, S. and Will, Y. 2009. Current Concepts in Drug-Induced Mitochondrial Toxicity. Current Protocols in Toxicology. 40:2.15:2.15.1–2.15.9.

Author Information

  1. Pfizer Inc., Groton, Connecticut

Publication History

  1. Published Online: 1 MAY 2009
  2. Published Print: MAY 2009


Mitochondria generate most of the cell's ATP and play key roles in fatty acid oxidation, steroid synthesis, heme synthesis, thermogenesis, calcium homeostasis, and apoptosis. With the development of new methods to study mitochondrial function, it is becoming clear that drug-induced mitochondrial dysfunction is one of the causes of drug toxicity. Mitochondria can be impaired by drugs in a variety of ways. These include inhibition of oxidative phosphorylation, uncoupling of electron transport from ATP synthesis, irreversible opening of the mitochondrial permeability transition pore, inhibition of transporters within the mitochondrial inner membrane, increased oxidative stress, inhibition of the citric acid cycle, inhibition of fatty acid oxidation, and impairment of either mtDNA replication or mtDNA-encoded protein synthesis. This unit provides an overview on the physiological roles of mitochondria and the mechanisms by which they can be adversely affected by drugs. Curr. Protoc. Toxicol. 40:2.15.1-2.15.9. © 2009 by John Wiley & Sons, Inc.


  • toxicity;
  • mitochondria;
  • energy production;
  • ROS;
  • apoptosis;
  • mtDNA;
  • mt ribosomes;
  • drug toxicity