Plasmalogen phospholipids in plasma lipoproteins of normolipidemic donors and patients with hypercholesterolemia treated by LDL apheresis

• Published in: Atherosclerosis 1996-01, Vol.119 (1), p.77-88
• Main Authors: Bräutigam, Carola, Engelmann, Bernd, Reiss, Daniela, Reinhardt, Ulrike, Thiery, Joachim, Richter, Werner O., Brosche, Thorolf
• Format: Article
• Language: English
• Subjects: Adult; Alpha tocopherol; Biological and medical sciences; Blood Component Removal; Female; General and cellular metabolism. Vitamins; HDL; Humans; Hypercholesterolemia - blood; Hypercholesterolemia - therapy; Lipoproteins - blood; Lipoproteins - chemistry; Lipoproteins, LDL - blood; Male; Medical sciences; Middle Aged; Pharmacology. Drug treatments; Phospholipids - blood; Plasmenylcholine; Plasmenylethanolamine; Polyunsaturated fatty acids; Red blood cell membranes
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/0021-9150(95)05632-7

Recent evidence indicates that plasmalogen phospholipids are particularly sensitive to oxidation and may possess antioxidative properties. Approximately 4.4%–5.5% of phosphatidylcholine (PC), and 53%–60% of phosphatidylethanolamine (PE) consisted of the plasmalogen phospholipids, plasmenylcholine and plasmenylethanolamine, respectively, in whole plasma, low density lipoprotein (LDL) and high density lipoprotein (HDL) of 11 normolipidemic donors. Of total plasmalogen phospholipids in plasma, slightly more was associated with LDL particles (about 42%) than with HDL (36%). Plasmalogen phospholipid levels were analyzed in 12 patients with familial hypercholesterolemia (FH) regularly treated by LDL apheresis, of whom 6 were supplemented with vitamin E (alpha tocopherol, 400 IU/day), the remaining 6 not receiving the antioxidant. Before apheresis (pre), total plasmalogen phospholipid levels in plasma and LDL (expressed as μmol/mmol cholesterol of compartment) decreased as follows: patients receiving vitamin E > normolipidemia > patients not receiving vitamin E. In both hypercholesterolemic groups, the contents of plasmalogen phospholipids in whole plasma and LDL were 3–5-fold higher than those of vitamin E. Directly after apheresis (post), plasmalogen phospholipid levels in plasma were raised by about 50% in the two hypercholesterolemic groups, mostly due to increases in plasmenylethanolamine levels. Two days after apheresis (48 h post), plasmalogen contents were still elevated in plasma and red blood cell membranes of patients receiving vitamin E, while they had already reached pre-apheresis values in those not supplemented with alpha tocopherol. Molecular species of plasma diacyl phospholipids containing polyunsaturated fatty acids were elevated at pre in patients receiving vitamin E as compared to patients without supplementation. At 48 h post, LDL apheresis induced an increase in these molecular species only in patients receiving vitamin E. In conclusion, the contents of plasmalogen phospholipids in plasma lipoproteins are at least three times higher than those of vitamin E. LDL apheresis raises the level of plasmalogen phospholipids in plasma, the increase persisting longer in patients supplemented with vitamin E. Supplementation with vitamin E appears to protect plasmalogen phospholipids in plasma lipoproteins against oxidative degradation.