Distribution of fatty acids of plasmalogenic phospholipids in human erythrocytes
and endometrium under hyperplasia of various character
It is shown that development of hyperplasia of endometrium (PPPE) is accompanied by the valid decrease of plasmenyl-phosphatidylethanolamine (PL PhEA) amount both in the blood erythrocytes and human endometrium and by the increase of diacylglycerophosphoethanolamin (DG PhEA). Data obtained evidence for the development of the state of plasmalogenic phospholipids insufficiency in the organism. When investigating the composition and quantity of fatty acids of plasmalogenic phospholipids of PhEA in the blood erythrocytes of patients it was established that the amount of arachidonic (C 20:4 ?-6) and docosahexaenoic (C 22:6 ?-3) reliably decreases more than by 50%. At the same time one can observe the reliable increase of palmitic (C 16:0) and stearic (C 18:0) fatty acids. Under these conditions the ratios ?-6/?-3 of both arahidonic and docosahexaenoic (AA/DHA) PL PhEA in the composition of erythrocyte PhEA increase with hyperplasia development 4 and 2 times respectively, but in DPhG the above ratios decreased 1.5 times. The decrease of PUFA in erythrocytes evidences for the increase of their use for restoration of their level disturbances in the organism. As a result of analysis of fatty acids content in tissues at hyperplasia development, considerable decrease of AA and DHA was established in one group of examined patients compared with the control, as well as the increase of ?-6/?-3 2.8 times, and AA/DHA 2 times. Reliable double increase of AA and eicosatrienoic acid and decrease of DHA and linolenic acid was observed in group 2 of the patient with adenomatosic hyperplasia. The ratio ?-6/?-3 and AA/DHA decreased twice in the both groups as compared with the control, that evidenced for development of hyperplasia of different origin. Specific distribution of arachidonic acid in plasmalogenic phospholipids at adenomatosic hyperplasia is connected with decrease of plasmalogens content and increase of formation of prostaglandin E2.
Published at the site: 2004-06-06
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