DELAYED OXIDATIVE-DEGRADATION OF POLYUNSATURATED DIACYL PHOSPHOLIPIDSIN THE PRESENCE OF PLASMALOGEN PHOSPHOLIPIDS IN-VITRO

The oxidative degradation of plasmalogen (alkenylacyl) phospholipids w as analysed in the absence and the presence of polyunsaturated ester p hospholipids by H-1-NMR and by chemical determination. Brain lysoplasm enylethanolamine (lyso-P-PE), brain P-PE and erythrocyte P-PE, contain ing an increasing number of intrachain double bonds at sn(2), were oxi dized with 2,2'-azobis-(2-amidinopropane hydrochloride) (AAPH; 2 or 10 mM) in Triton X-100 micelles (detergent/phospholipid 1:5, mol/mol). T he formation of two peroxyl radicals was accompanied by the degradatio n of approx. one molecule of brain lyso-P-PE. On oxidation of brain P- PE or erythrocyte P-PE(320 nmol) with 2 mM AAPH, the (alpha-vinyl) met hine H-1 signal of the enol ether decreased more rapidly than the meth ine proton peak of intrachain double bonds. The rate of enol ether deg radation increased in the order: erythrocyte P-PE > brain P-PE > brain lyso-P-PE. The disappearance of the polyunsaturated ester phospholipi ds 1-palmitoyl-2-arachidonoyl phosphatidylcholine (16:0/20:4-PC) and 1 -palmitoyl-2-linoleoyl phosphatidylcholine (16:0/18:2-PC) (100 nmol), as induced by 10 mM AAPH, was nearly completely inhibited by the plasm alogens (25 nmol) in the first 30 and 60 min of incubation respectivel y, and was delayed at later time points. Plasmalogens and vitamin E (4 -25 nmol) mitigated the decreases in 16:0/[H-3]20:4-PC (100 nmol) indu ced by 2 mM AAPH in a similar manner. The initial rate of degradation of intrachain double bonds of 16:0/20:4-PC and 16:0/18:2-PC (320 nmol; 2 mM AAPH) was decreased by 59 % and 81 % respectively in the presenc e of 80 nmol of brain lyso-P-PE. In conclusion, plasmalogens markedly delay the oxidative degradation of intrachain double bonds under in vi tro conditions. Interactions of enol ether double bonds with initiatin g peroxyl radicals as well as with products generated by prior oxidati on of polyunsaturated fatty acids are proposed to be responsible for t his capacity of plasmalogens. Furthermore, the products of enol ether oxidation apparently do not propagate the oxidation of polyunsaturated fatty acids.