Journal
PHARMACOLOGY & THERAPEUTICS
Volume 99, Issue 1, Pages 45-53Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0163-7258(03)00052-4
Keywords
amphetamine; mitochondria; free radicals; oxidative stress; reactive oxygen species; reactive nitrogen species
Categories
Funding
- NIDA NIH HHS [DA07606] Funding Source: Medline
Ask authors/readers for more resources
Amphetamine-like psychostimulants are associated with long-term decreases in markers for monoaminergic neurons, suggesting neuronal loss and/or damage within the brain. This long-term toxicity results from formation of free radicals, particularly reactive oxygen species (ROS) and reactive nitrogen species (RNS), although the mechanism(s) of ROS and RNS formation are unclear. Mitochondria are a major source of ROS and mitochondrial dysfunction has been linked to some neurodegenerative disorders. Amphetamines also inhibit mitochondrial function, although the mechanism involved in the inhibition is,uncertain. This review coordinates findings on the multiple pathways for ROS and RNS and describes a hypothesis. involving mitochondrial inhibition in the initiation of amphetamine-induced cellular necrosis. (C) 2003 Elsevier Science Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available