Modulation by dietary oils and clofibric acid of arachidonic acid content in phosphatidylcholine in liver and kidney of rat: effects on prostaglandin formation in kidney.
The manipulation of 20:4(n - 6) contents in phosphatidylcholine of liver and kidney of rats by dietary oils and p-chlorophenoxyisobutyric acid (clofibric acid) as well as the effects on the formation of prostaglandin E2 in kidney were studied. Three groups of rats were fed diets that contained either safflower oil (SO) or perilla oil (PO) or fish oil (FO) for 1 week. Each dietary group was divided into two groups. One group continued the same diet for another 1 week; the second group continued the same diet and received subcutaneous injections of clofibric acid once a day for 1 week. The content of 20:4(n - 6) in hepatic phosphatidylcholine was markedly lowered by feeding either FO or PO and was further decreased by the administration of clofibric acid. Feeding either FO or PO lowered the content of 20:4(n - 6) in hepatic phosphatidylethanolamine, whereas clofibric acid increased it. The decrease in the level of 20:4(n - 6) in serum phospholipid was produced by feeding either FO or PO and by the administration of clofibric acid as well. There was a high correlation for the levels of 20:4(n - 6) between hepatic phosphatidylcholine and serum phospholipid. The changes brought about by dietary oils and clofibric acid in renal phosphatidylcholine was similar to those observed in liver. The content of 20:4(n - 6) in renal phosphatidylcholine was highly correlated with the level of 20:4(n - 6) in serum phospholipid. Other phospholipids in kidney responded less sensitively to the manipulation by dietary oils and clofibric acid. These results suggest that the level of 20:4(n - 6) in renal phosphatidylcholine is regulated by the level of 20:4(n - 6) in hepatic phosphatidylcholine through the changes in serum level of 20:4(n - 6). Formation of prostaglandin E2 in kidney slices was dependent on the content of 20:4(n - 6) in renal phosphatidylcholine.
Kawashima
Y
Y
Faculty of Pharmaceutical Sciences, Toyama Medical and Pharmaceutical University, Japan.
Mizuguchi
H
H
Kozuka
H
H
D000818:Animals; D016718:Arachidonic Acid / Q000032:analysis*; D002995:Clofibric Acid / Q000494:pharmacology*; D015232:Dinoprostone / Q000096:biosynthesis*; D005395:Fish Oils / Q000494:pharmacology*; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008041:Linoleic Acids / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010713:Phosphatidylcholines / Q000097:blood / Q000737:chemistry*; D010743:Phospholipids / Q000097:blood / Q000737:chemistry; D010938:Plant Oils / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012450:Safflower Oil / Q000494:pharmacology*; D017962:alpha-Linolenic Acid
D005395:Fish Oils; D008041:Linoleic Acids; D010713:Phosphatidylcholines; D010743:Phospholipids; D010938:Plant Oils; D017962:alpha-Linolenic Acid; D016718:Arachidonic Acid; D002995:Clofibric Acid; C058216:perilla seed oil; D012450:Safflower Oil; D015232:Dinoprostone