Platelet phospholipids are differentially protected against oxidative degradation by plasmalogens.

The oxidative degradation of phospholipids in the presence and absence of plasmalogens (plasmenyl phosphatidylethanolamine: PPE) was followed by chemical analysis. Human platelet phospholipids, either intact or after removal of PPE by acid treatment, were oxidized with 28 mM 2,2'-azobis(2-amidinopropane di-HCl in Triton X-100 micelles (detergent/phospholipid 5:1, mol/mol). PPE (12% of all phospholipids, mol/mol) disappeared about three times more rapidly than glycerophospholipids, whereas sphingomyelin remained unaltered and the lysophosphatidylethanolamine (lysoPE) generated became progressively more unsaturated. After 60 min oxidation, the FA compositions of PS, PC, and PI were similar in extracts with or without plasmalogens. In contrast, diacyl phosphatidylethanolamine (DPE) became more saturated in the absence of PPE. The rate of phospholipid destruction was always unique to each class, but for all phospholipids slowed down in the presence of PPE. This protective effect increased in the order DPE < PS < PC < PI and did not seem to be simply related to the class unsaturation. Alpha-tocopherol had no influence on the time courses of the quantities and compositions of the phospholipids, even at a molar ratio of alpha-tocopherol to phospholipids four times higher than in platelet membranes. Thus, PPE protected phospholipids efficiently but differentially against peroxidative attack, whereas the contribution of alpha-tocopherol appeared to be negligible even at a concentration four times greater than in platelet membranes.