Open AccessMitochondrial Toxicity of Drugs
Author(s) -
Liliane Todesco,
Katri Waldhauser,
Stephan Krähenbühl
Publication year - 2006
Publication title -
chimia
Language(s) - English
Resource type - Journals
eISSN - 2673-2424
pISSN - 0009-4293
DOI - 10.2533/000942906777675083
Subject(s) - mitochondrial permeability transition pore , toxicity , mitochondrion , apoptosis , oxidative phosphorylation , microbiology and biotechnology , chemistry , necrosis , inner mitochondrial membrane , membrane permeability , oxidative damage , electron transport chain , membrane , oxidative stress , pharmacology , biochemistry , biology , programmed cell death , genetics , organic chemistry
Mitochondria are important targets of drug toxicity. A variety of drugs has been shown to affect the electron transport chain, coupling of oxidative phosphorylation, ?-oxidation or other mitochondrial functions. Such damaging events may lead to the opening of a large pore across the mitochondrial membranes – the membrane permeability transition pore – eventually leading to apoptosis or necrosis of cells, depending on the cellular ATP content. Such drugs may therefore lead to organ damage, particularly in the liver, kidney, heart or skeletal muscle.