Lung, aorta, and platelet metabolism of 14C-arachidonic acid in vitamin E deficient rats.
14C-arachidonic acid metabolism was determined in aortas, platelets, and perfused lungs from rats pair fed a basal diet supplemented with 0 or 100 ppm vitamin E for 11 weeks. Spontaneous erythrocyte hemolysis tests showed 92% and 8% hemolysis for the 0 and 100 ppm vitamin E groups, respectively. Elevated lung homogenate levels of malonaldehyde in the 0 ppm group confirmed its deficient vitamin E status. Aortas from the vitamin E deficient group synthesized 54% less prostacyclin than aortas from the supplemented group (p less than 0.05). Although thromboxane generation by platelets from the vitamin E deficient group exhibited a 37% increase, this difference was not statistically significant compared to the supplemented animals. Greater amounts of PGE2, PGF2 alpha, TXB2, and 6-keto-PGF1 alpha were obtained in albumin buffer perfusates from lungs of vitamin E deficient rats than in those from supplemented rats. Significant differences (p less than 0.05) were noticed, however, only for PGE2 and PGF2 alpha. These studies indicate that vitamin E quantitatively alters arachidonic acid metabolism in aortic and lung tissue but its effect on thromboxane synthesis by platelets is less marked.
D000818:Animals; D001011:Aorta / Q000378:metabolism*; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism*; D001792:Blood Platelets / Q000378:metabolism*; D002250:Carbon Radioisotopes; D011464:Epoprostenol / Q000378:metabolism; D006461:Hemolysis / Q000187:drug effects; D066298:In Vitro Techniques; D007700:Kinetics; D008054:Lipid Peroxides / Q000378:metabolism; D008168:Lung / Q000378:metabolism*; D008297:Male; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D014810:Vitamin E / Q000494:pharmacology; D014811:Vitamin E Deficiency / Q000378:metabolism*
D001095:Arachidonic Acids; D002250:Carbon Radioisotopes; D008054:Lipid Peroxides; D014810:Vitamin E; D016718:Arachidonic Acid; D011464:Epoprostenol