Evaluation of the concomitance of lipid peroxidation in experimental models of cerebral ischemia and stroke

Brant D. Watson

Research output: Contribution to journalArticlepeer-review

72 Scopus citations

Abstract

This chapter discusses an important consequence of oxygen radical formation: lipid peroxidation. Lipid peroxidation arises during and following disruption of membrane structure via oxygen-consuming rancidity reactions. Membrane viscosity and rigidity are increased and microscopically visible fissures or holes are formed in the membrane lipid bilayer. Consistent with these defects are reports of enhanced permeability and the development of edema. Lipid peroxidation can inhibit the function of important membrane-bound enzymes as well. For example, the hydroperoxide formed from arachidonic acid inhibits endothelial prostacyclin synthase, thereby inactivating an important response of endothelium to aggregating platelets. Lipid peroxides are chemically unstable and can continue to degrade into many other products, which are also chemically reactive. In particular, reactive species such as aldehydes can be produced; these can also induce changes in membrane structure and function by cross-linking amino groups of proteins or polar head groups of phospholipid molecules. Lipid peroxidation is damaging to tissues principally because it is a chain process; a single initiating free radical can precipitate the destruction of many adjacent molecules in a cellular structure and thus compromise its function.

Original languageEnglish (US)
Pages (from-to)69-95
Number of pages27
JournalProgress in brain research
Volume96
Issue numberC
DOIs
StatePublished - Jan 1 1993

ASJC Scopus subject areas

  • Neuroscience(all)

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