Dopamine metabolism and free-radical related mitochondrial injury during transient brain ischemia in gerbils

Regional extracellular release of dopamine (DA) and its metabolites, 3,4-dihydroxy-phenylacetic acid (DOPAC), homovanillic acid (HVA) and 3-methoxytyramine (3-MT) was measured in gerbils (with or without pargyline pretreatment) subjected to bilateral carotid artery occlusion (15 min) and various per...

Full description

Saved in:
Bibliographic Details
Published in:Neurochemical research 1993-11, Vol.18 (11), p.1193-1201
Main Authors: ISHII, H, STANIMIROVIC, D. B, CHANG, C. J, MRSULJA, B. B, SPATZ, M
Format: Article
Language:English
Subjects:
3,4-Dihydroxyphenylacetic Acid - metabolism
Animals
Biological and medical sciences
Chromatography, High Pressure Liquid
Dialysis
Dopamine - analogs & derivatives
Dopamine - metabolism
Free Radicals
Gerbillinae
Homovanillic Acid - metabolism
Ischemic Attack, Transient - metabolism
Ischemic Attack, Transient - pathology
Lipid Peroxidation
Medical sciences
Meriones unguiculatus
Mitochondria - metabolism
Monoamine Oxidase - metabolism
Neurology
Pargyline - pharmacology
Superoxide Dismutase - metabolism
Thiobarbituric Acid Reactive Substances - metabolism
Vascular diseases and vascular malformations of the nervous system
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Regional extracellular release of dopamine (DA) and its metabolites, 3,4-dihydroxy-phenylacetic acid (DOPAC), homovanillic acid (HVA) and 3-methoxytyramine (3-MT) was measured in gerbils (with or without pargyline pretreatment) subjected to bilateral carotid artery occlusion (15 min) and various periods of recirculation (up to 6 hr), utilizing intracerebral microdialysis and high-performance liquid chromatography (HPLC) with electrochemical detection. Mitochondrial monoamine oxidase (MAO) and superoxide dismutase (SOD) activities and in vitro stimulated lipid peroxidation (TBARM) were determined in separate experimental groups of animals. The ischemically induced DA release, decrease of MAO-derived DA metabolites DOPAC and HVA, and accumulation of 3-MT were potentiated and prolonged by pargyline pretreatment. Mitochondrial MAO and SOD activities were significantly reduced during ischemia alone and up to 1 hr of reperfusion, whereas TBARM was enhanced during reflow only. The data suggest that reduced activity of mitochondrial antioxidative enzyme(s) but not DA metabolism by MAO may contribute to free radical-mediated injury of (mitochondrial) membranes.
ISSN:0364-3190
1573-6903
DOI:10.1007/bf00978373