Low density lipoproteins (LDL) are carriers for lipid peroxides and inhibit prostacyclin (PGI2) biosynthesis in arteries.
Serum lipid peroxides are concentrated in the LDL fraction. HDL and plasma proteins quench the interaction of LDL lipid peroxides with thiobarbituric acid. LDL inhibits prostacyclin biosynthesis both in incubated rat aortic slices and superfused bovine coronary arteries. It is proposed that atherogenic properties of LDL are associated with inactivation of arterial prostacyclin synthetase by lipid peroxides which are present in LDL.
D000818:Animals; D001158:Arteries / Q000378:metabolism*; D002417:Cattle; D002914:Chylomicrons / Q000032:analysis; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D006951:Hyperlipoproteinemias / Q000097:blood; D008054:Lipid Peroxides / Q000032:analysis*; D008075:Lipoproteins, HDL / Q000032:analysis; D008077:Lipoproteins, LDL / Q000032:analysis* / Q000494:pharmacology; D008079:Lipoproteins, VLDL / Q000032:analysis; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats
D002914:Chylomicrons; D008054:Lipid Peroxides; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D011453:Prostaglandins; D011464:Epoprostenol