The activity of hepatic lysophospholipid acyltransferase in zinc-deficient rats

Recent studies have demonstrated that zinc deficiency increases the levels of long chain n-3 polyunsaturated fatty acids (PUFA) and reduces the levels of n-6 PUFA in rat tissues (Eder and Kirchgessner 1994a,b, 1995). In particular, the ratio between eicosapentaenoic acid (EPA) and arachidonic acid (AA) in tissue phospholipids, particularly in phosphatidylcholine was markedly elevated by zinc deficiency. The ratio between these fatty acids is of great physiologic relevance because eicosanoids produced from EPA and AA mediate physiological processes in diverse ways. For instance, in platelets, AA is metabolized primarily to thromboxane A₂ which is a potent stimulant of platelet aggregation and a vasoconstrictor. In contrast, EPA is converted to small amounts of thromboxane A₃ which is a poor agonist for inducing platelet aggregation (Sprecher 1986).
To date, the reason for the increased ratio between n-3 PUFA and n-6 PUFA in zinc-deficient animals is unknown. One possible reason, however, could be an altered incorporation of PUFA into phospholipids by lysophospholipid acyltransferase. This enzyme reacylates lysophospholipids and hence, is the key enzyme in phospholipid renewal. The present study was conducted to investigate whether an altered activity of this enzyme could be the reason for the altered fatty acid composition of membrane phospholipids observed in zinc-deficient rats. As previous studies (Eder and Kirchgessner 1994a, 1995, 1997) have demonstrated that the type of fat influences the effects of zinc deficiency on the fatty acid metabolism, the study used two different fat sources, olive oil with a high level of mono-unsaturated fatty acids (MUFA) and linseed oil with a high level of n-3 PUFA.