Prevention of Liver Cell Damage Following Lipid Peroxidation by Depression of Lysophosphatide Formation
In hepatocytes cytotoxic events induced by haloalkanes or acute iron-overload exhibit neither a quantitative nor a temporal correlation to lipid peroxidation (Ungemach 1987). This is contradictory to the unicausal theory of liver cell necrosis as a direct consequence of the peroxidative destruction of polyunsaturated fatty acids in biological membranes. Thus, secondary toxicological mechanisms have been postulated (Recknagel 1983). As a relevant secondary pathological mechanism an autocatalytic activation of phospholipase A2 could be demonstrated which is triggered by lipid peroxidation and finally produces cytolytic amounts of lysophosphatides in the plasma membrane (Ungemach 1987). If this concept of phospholipase A2 activation represents a significant lipid peroxidation-dependent cytotoxic mechanism, it has to be assumed that under conditions of phospholipase A inhibition or suppression of the formation of critical lysophosphatide concentrations the late membrane damage of hepatocytes may be prevented.
KeywordsDepression Manifold Lipase Choline Diene
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