Albumin stimulates the release of arachidonic acid from phosphatidylcholine in hamster lungs.
14C-Arachidonic acid injected into the pulmonary circulation of isolated hamster lungs was effectively incorporated into lung lipids. Once retained the radiolabel was relatively stable but the release of radioactivity increased up to 10-fold when bovine serum albumin (1%) was added to the perfusate. This efflux of radioactivity was not blocked by quinacrine, a phospholipase A2 inhibitor. In albumin experiments the released 14C-arachidonate originated mainly from the phospholipid fraction in which phosphatidylcholine was the main source of the released radioactivity. Pulmonary infusion of albumin had no significant effect on the amount of 14C-arachidonic acid in the neutral lipid or free fatty acid fractions of perfused lungs. In experiments with albumin about 80% of the released radioactivity co-chromatographed with unlabelled arachidonic acid whereas in the absence of albumin only about 20% of the released radioactivity was unmetabolized arachidonic acid. This study indicates that albumin stimulates the release of arachidonic acid from isolated hamster lungs and that the release is increased mainly from the phosphatidylcholine fraction.
D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D008168:Lung / Q000378:metabolism*; D008297:Male; D010713:Phosphatidylcholines / Q000378:metabolism*; D011796:Quinacrine / Q000494:pharmacology; D012710:Serum Albumin, Bovine / Q000494:pharmacology*
D001095:Arachidonic Acids; D010713:Phosphatidylcholines; D012710:Serum Albumin, Bovine; D016718:Arachidonic Acid; D011796:Quinacrine