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Metabolism of 1,2‐(1‐ 14 C) dipalmitoyl phosphatidylcholine in the developing brain
Author(s) -
Dhopeshwarkar G. A.,
Subramanian Carole,
Mead James F.
Publication year - 1973
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/bf02531844
Subject(s) - phosphatidylcholine , chemistry , chromatography , phospholipid , lecithin , phosphatidylethanolamine , fatty acid , biochemistry , metabolism , phospholipase , palmitic acid , enzyme , membrane
Thirteen‐day‐old rats were divided into two groups; one group received 1,2‐(1‐ 14 C) dipalmitoyl phosphatidylcholine and the other 1‐ 14 C palmitic acid in the form of an intraperitoneal injection. One half of the total number of rats in each group was sacrificed 24 hr after injection, and the other half was allowed to survive for 17 days after the injection. Radioactivity incorporated into brain and liver total lipids and into individiual polar lipid components of the brain was determined at both intervals. Phosphatidylcholine was isolated and partially deacylated with phospholipase A 2 from Crotalus Admanteus venom. The ratio of radioactivity FA 2/FA 1 (fatty acid attached to 2 and 1 carbon of the glycerol moiety) 24 hr after the injection was 8.3, when the tracer was radioactive phosphatidylcholine, compared to only 0.7 when radioactive palmitate was injected. From this different labeling ratio and different pattern of labeling the polar lipid components, it was concluded that the radioactive phosphatidylcholine was not deacylated completely before being taken up directly into the brain. Possibilities are discussed to show that the observed radioactive ratio could result from direct uptake of intact phosphatidylcholine, with little or no restriction from the blood brain barrier system, followed by partial degradation by phospholipase A 1 in the brain itself.