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Free radicals and brain damage

Siesjö, Bo LU ; Agardh, Carl-David LU and Bengtsson, F (1989) In Cerebrovascular and Brain Metabolism Reviews 1(3). p.165-211
Abstract
Although free radicals have been suggested to contribute to ischemic brain damage for more than 10 years, it is not until quite recently that convincing evidence has been presented for their involvement in both sustained and transient ischemia. The hypothesis is examined against current knowledge of free radical chemistry, as it applies to biological systems, and of cellular iron metabolism. It is emphasized that those advents have changed our outlook on free radical-induced tissue damage. First, it has been realized that damage to DNA and proteins may be an earlier event than lipid peroxidation, perhaps also a more important one. Second, evidence now exists that the triggering event in free radical-induced damage is a disturbance of... (More)
Although free radicals have been suggested to contribute to ischemic brain damage for more than 10 years, it is not until quite recently that convincing evidence has been presented for their involvement in both sustained and transient ischemia. The hypothesis is examined against current knowledge of free radical chemistry, as it applies to biological systems, and of cellular iron metabolism. It is emphasized that those advents have changed our outlook on free radical-induced tissue damage. First, it has been realized that damage to DNA and proteins may be an earlier event than lipid peroxidation, perhaps also a more important one. Second, evidence now exists that the triggering event in free radical-induced damage is a disturbance of cellular iron metabolism, notably delocalization of protein-bound iron, and its chelation by compounds that trigger site-specific free radical damage. Third, methods have been developed that allow the demonstration of partially induced oxygen species in tissues, and scavengers have become available that can curb free radical reactions. As a result of these events, it has been possible to demonstrate formation of free radicals in oxygen toxicity, trauma, and ischemia, and their participation in the cell damage that is incurred in these conditions, particularly in causing vascular pathology and edema. It is suggested that in ischemia, free radical damage becomes pathogenetically important when the ischemia is of long duration, when conditions favor continued delivery of some oxygen to the ischemic tissue, and particularly when such partially oxygen-deprived tissue is reoxygenated. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cerebrovascular and Brain Metabolism Reviews
volume
1
issue
3
pages
165 - 211
publisher
Raven Press
external identifiers
  • pmid:2701375
  • scopus:0024722019
ISSN
1040-8827
language
English
LU publication?
yes
id
e57745f2-0107-45ce-b0c7-06dbf0c5b492 (old id 1104582)
date added to LUP
2008-08-06 11:12:59
date last changed
2017-08-13 04:18:56
@article{e57745f2-0107-45ce-b0c7-06dbf0c5b492,
  abstract     = {Although free radicals have been suggested to contribute to ischemic brain damage for more than 10 years, it is not until quite recently that convincing evidence has been presented for their involvement in both sustained and transient ischemia. The hypothesis is examined against current knowledge of free radical chemistry, as it applies to biological systems, and of cellular iron metabolism. It is emphasized that those advents have changed our outlook on free radical-induced tissue damage. First, it has been realized that damage to DNA and proteins may be an earlier event than lipid peroxidation, perhaps also a more important one. Second, evidence now exists that the triggering event in free radical-induced damage is a disturbance of cellular iron metabolism, notably delocalization of protein-bound iron, and its chelation by compounds that trigger site-specific free radical damage. Third, methods have been developed that allow the demonstration of partially induced oxygen species in tissues, and scavengers have become available that can curb free radical reactions. As a result of these events, it has been possible to demonstrate formation of free radicals in oxygen toxicity, trauma, and ischemia, and their participation in the cell damage that is incurred in these conditions, particularly in causing vascular pathology and edema. It is suggested that in ischemia, free radical damage becomes pathogenetically important when the ischemia is of long duration, when conditions favor continued delivery of some oxygen to the ischemic tissue, and particularly when such partially oxygen-deprived tissue is reoxygenated.},
  author       = {Siesjö, Bo and Agardh, Carl-David and Bengtsson, F},
  issn         = {1040-8827},
  language     = {eng},
  number       = {3},
  pages        = {165--211},
  publisher    = {Raven Press},
  series       = {Cerebrovascular and Brain Metabolism Reviews},
  title        = {Free radicals and brain damage},
  volume       = {1},
  year         = {1989},
}