Incorporation of linoleic acid into membrane glycerophospholipids from rat brain submitted to ischemia and hypoxia.

In the presence of ATP, Mg and CoA-SH]1-14C]linoleic acid was incorporated into membrane phospholipids (P2 fraction and synaptosomes) prepared from rat brain cortex. The relative order for linoleate incorporation was: phosphatidyl-choline greater than phosphatidylethanolamine greater than phosphatidylinositol greater than ethanolamine plasmalogen greater than phosphatidylserine. The incorporation of labeled linoleate into P2 fraction phospholipids was investigated in rats, aged 4, 16, and 90 days, after being subjected to ischemic and hypoxic conditions. With the exception of a small increase in the incorporation of the radioactivity into diacyl-GPC, little change in incorporation profile was observed with 4-day-old rats submitted to ischemic and hypoxic conditions. However, the incorporation of labeled linoleate into membrane phospholipids was decreased in 16- and 90-day-old rats being subjected to ischemic and hypoxic conditions. Among the phospholipids, the decrease in incorporation of radioactivity was most prominent with ethanolamine plasmalogens and phosphatidylinositol, although the radioactivity of phosphatidylcholine seemed to remain relative constant. The decreased incorporation activity in these two age groups was noted along with concomitant increase in the FFA content, whereas in FFA was not observed in the 4-day-old brain samples. Thus, the specific decrease in labeling of ethanolamine plasmalogens and phosphatidylinositol may be the result of increased enzymic degradation of these compounds after ischemic and hypoxic treatment. Furthermore, the decrease in incorporation of linoleate into membrane phospholipids may be due to an increase in the membrane FFA pool which subsequently gave a dilution of the labeled precursor.