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Arachidonyl transfer from diacyl phosphatidylcholine to ether phospholipids in rat platelets.

ABSTRACT: High levels of ether phospholipids were found in rat platelets. Alkylacyl compounds constituted 18 and 29% of glycerophosphocholine (GPC) and glycerophosphoethanolamine (GPE). Alkenylacyl compounds, not detected in GPC, represented 40% of GPE. Arachidonate comprised 60%, 42% and 26% of the acyl residues in the sn-2 position of alkenylacyl-GPE, alkylacyl-GPE and alkylacyl-GPC respectively. Based on all arachidonate being linked to the sn-2 position of the diacyl species, the arachidonate level was 47% in diacyl-GPE and 30% in diacyl-GPC. The incorporation and metabolic fate of arachidonate in various phospholipid classes of resting platelets was examined. Arachidonate was essentially recovered in the diacyl phospholipids and very poorly in alkylacyl- and alkenylacyl-GPE and GPC after 30 min incubation in the presence of [14C]arachidonic acid. Upon reincubation of the platelets after removal of free arachidonate, the radioactivity was gradually lost from diacyl-GPC. Concomitantly, the radioactivities in alkylacyl-GPC, alkylacyl-GPE, alkenylacyl-GPE and to a lower extent in diacyl-GPE were increased. Labelling of glycerophosphoinositol was not changed. This labelling transfer was linear up to 5-6 h, except for alkylacyl-GPC; then labelling remained constant. These data strongly suggest that free arachidonate incorporation through the Lands pathway occurs only for diacyl species and that arachidonate incorporation into the ether phospholipids is achieved by exchange from diacyl-GPC. Based on specific activities related to phosphorus content, the arachidonate incorporation rates into diacyl-GPE and diacyl-GPC were approximately equivalent. The very large differences between specific radioactivities related to arachidonate observed at the starting reincubation time were strongly attenuated when labelling equilibrium was reached. The turnover rate by this exchange pathway was higher in alkylacyl-GPC than in alkyl- and alkenylacyl-GPE. This finding agrees with the selectivity for arachidonate observed in the acylation of PAF-acether in human neutrophils [Chilton, O'Flaherty, Ellis, Swendsen & Wykle (1983) J. Biol. Chem. 258, 7268-7271].

SUBMITTER: Colard O

PROVIDER: S-EPMC1144227 | biostudies-other | 1984 Sep

REPOSITORIES: biostudies-other

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Project description:The oxidative degradation of plasmalogen (alkenylacyl) phospholipids was analysed in the absence and the presence of polyunsaturated ester phospholipids by 1H-NMR and by chemical determination. Brain lysoplasmenylethanolamine (lyso-P-PE), brain P-PE and erythrocyte P-PE, containing an increasing number of intrachain double bonds at sn2, were oxidized with 2,2'-azobis-(2-amidinopropane hydrochloride) (AAPH; 2 or 10 mM) in Triton X-100 micelles (detergent/phospholipid 1:5, mol/mol). The formation of two peroxyl radicals was accompanied by the degradation 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) methine 1H signal of the enol ether decreased more rapidly than the methine proton peak of intrachain double bonds. The rate of enol ether degradation increased in the order: erythrocyte P-PE>brain P-PE>brain lyso-P-PE. The disappearance of the polyunsaturated ester phospholipids 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 plasmalogens (25 nmol) in the first 30 and 60 min of incubation respectively, and was delayed at later time points. Plasmalogens and vitamin E (4-25 nmol) mitigated the decreases in 16:0/[3H]20:4-PC (100 nmol) induced 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 presence of 80 nmol of brain lyso-P-PE. In conclusion, plasmalogens markedly delay the oxidative degradation of intrachain double bonds under in vitro conditions. Interactions of enol ether double bonds with initiating peroxyl radicals as well as with products generated by prior oxidation of polyunsaturated fatty acids are proposed to be responsible for this capacity of plasmalogens. Furthermore, the products of enol ether oxidation apparently do not propagate the oxidation of polyunsaturated fatty acids.

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Arachidonyl transfer from diacyl phosphatidylcholine to ether phospholipids in rat platelets.

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