Reactive Oxygen Species in the Induction of Toxicity
Molecular and Cellular Aspects of Toxicology
Published Online: 15 DEC 2009
Copyright © 2009 John Wiley & Sons, Ltd. All rights reserved.
General, Applied and Systems Toxicology
How to Cite
Lenaz, G. and Strocchi, P. 2009. Reactive Oxygen Species in the Induction of Toxicity. General, Applied and Systems Toxicology. .
- Published Online: 15 DEC 2009
Oxidative stress is among the major causes of toxicity due to interaction of reactive oxygen species (ROS) with cellular macromolecules and structures and interference with signal transduction pathways. ROS originate from exogenous and endogenous sources; among the former are UV and ionizing radiation and xenobiotics, the latter are represented by a number of metabolic reactions. The mitochondrial respiratory chain, specially from Complexes I and III, is considered the main origin of ROS particularly under conditions of high membrane potential, but several other sources may be important for ROS generation, such as mitochondrial p66Shc, monoamine oxidase, α-ketoglutarate dehydrogenase and extramitochondrial xanthine oxidase, cytochrome P450, nitric oxide synthase, peroxisomal enzymes, plasma membrane NADPH oxidases, and lipoxygenase, with the participation of redox-active metal ions. ROS are able to oxidatively modify lipids, proteins, carbohydrates and nucleic acids and to activate/inactivate signalling pathways by oxidative modification of redox-active factors. Cells are endowed with several defence mechanisms, including repair or removal of damaged molecules, and antioxidant systems, either enzymatic or nonenzymatic. Oxidative stress is at the basis of ageing and many pathological disorders, such as ischaemic diseases, neurodegenerative diseases, diabetes and cancer, although the underlying mechanisms are not always completely understood.
- reactive oxygen species;
- ROS-generating reactions;
- respiratory complexes;
- oxidative stress;
- signal transduction;
- cellular toxicity