Lysophosphatidylcholine uptake and metabolism in the adult rabbit lung

Tracer quantities of 3H-labeled lysoPC and 32P-labeled natural rabbit surfactant were given intratracheally via a bronchoscope and [14C]palmitate was given intravenously to 25 rabbits with labeled PC and lysoPC measured in the alveolar wash, lung homogenate, lamellar bodies and microsomes at five times from 10 min to 6 h after tracheal injection. Surprisingly, only 31% of the administered lysoPC remained in its original form in the total lungs (alveolar wash + lung homogenate) by 10 min, of which 77% was in the alveolar wash. Meanwhile, by 10 min an additional 37% was already converted to PC, of which more than 98% was in the lung homogenate. LysoPC continued to be rapidly and efficiently converted to PC, with 62% conversion measured at 3 h. The converted lysoPC initially appeared with high specific activity in microsomes, then in lamellar bodies, and finally in the alveolar wash. The intravascular palmitate labeled lung PC had similar specific activity-time profiles in the subcellular fractions, while intratracheally administered natural rabbit surfactant had a constantly low specific activity in microsomes and much higher specific activities in lamellar bodies and alveolar wash. Another 25 rabbits received intratracheal lysoPC labeled in both the choline and palmitate moieties and then were studied from 1 to 24 h after tracheal injection. The ratio of the palmitate to choline labels indicated uptake and conversion to PC primarily by direct acylation rather than transacylation and by intact reuptake and conversion rather than breakdown and resynthesis. LysoPC is an attractive 'metabolic probe' of surfactant metabolism which undergoes very rapid and efficient intracellular conversion to PC via a subcellular pathway that parallels the remodeling and de novo synthetic pathways.     

Lipid metabolism by the gall-bladder. I. The in situ uptake and metabolism of lysophosphatidylcholine

Accumulation of lysophosphatidylcholine in gall-bladder bile is involved in the pathogenesis of acute cholecystitis. [1-14C]oleoyl- or [1-14C]palmitoyl-lysophosphatidylcholine was thus instilled in the in situ guinea pig gall-bladder and the absorption and metabolism of the lipid were determined. We found that, after 6 h instillation, 53% of the oleoyl derivative was adsorbed by the gall-bladder, whereasee only 37% of the palmitoyl derivative was absorbed. Although some differences in the metabolism of these two lipids were observed, a major portion of the absorbed radioactivity was found in the gall-bladder wall as phosphatidylcholine. To determine the mechanism of phosphatidylcholine formation from lysophosphatidylcholine by the gall-bladder mucosa, we used lysophosphatidylcholine which was labelled in the fatty acid moiety with 14C and in the choline moiety with 3H. Our data suggest that the mechanism of phosphatidylcholine formation from lysophosphatidylcholine involved acylation with an acyl donor other than a second molecule of lysophosphatidylcholine. We hypothesize that this mechanism as well as others described serve to prevent accumulation of lysophosphatidylcholine within the gall-bladder lumen and thus prevent damage to the gall-bladder mucosa.