Abstract

This article briefly reviews the importance and relevance of membrane lipid degradation to the pathogenesis of ischemic brain damage ranging from the liberation and accumulation of free fatty acids (FFA) to their consequences on the biophysical characteristics of membrane lipids. The rapid accumulation of brain FFA during cerebral ischemia is a hallmark of the evolution and pathogenesis of ischemic brain damage: It signals the degradation of membrane lipids; it generates the precursors to the metabolically and physiologically potent eicosanoids; and it promotes the generation of lipid oxidizing free radicals, which could propagate the destruction of membrane lipids. The impact of ischemia-induced changes in cerebral membrane lipid composition on membrane function is difficult to assess in vivo. Some estimate of the impact of the changes, however, can be obtained by evaluating the changes induced in the surface pressure-area diagrams (SPAD) of membrane lipid monolayers at the air-water interface. Lipid monolayers are used as model membranes to study the effects of lipid composition on the biophysical behavior of membrane lipids and their interaction. Regional brain lipids were quantitated at different times during ischemia, and their impact on their surface pressure area diagrams was assessed and their potential impact on membrane function discussed.

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