Antepartum administration of L-carnitine to pregnant rats results in an increase of both total phospholipid (80 ± 11 mg/g dry weight (dw); mean ± SD) and dipalmitoylphosphatidylcholine (DPPC) content (7.7 ± 2.1 mg/g dw) in fetal lungs as compared to controls (72 ± 10 and 7.0 ± 2.5 mg/g dw, respectively). On the other hand, no effect of L-carnitine could be demonstrated on the DPPC portion in the total phosphatidylcholine (PC) or on the portion of palmitic acid in the PC fatty acids.Betamethasone elevated the DPPC content in fetal lungs (8.1 ± 2.0 versus 7.0 ± 2.5 mg/g dw in the controls), while total phospholipid content remained unaffected (71 ± 19 versus 72 ± 10 mg/g dw). The portion of DPPC in the PC species increased significantly (p<0.01) from 27.6 ± 4.5 in the fetal lungs of the control group to 34.2 ± 3.3 in the lungs of the betamethasone-treated group, while the palmitic acid portion in the PC fatty acids was nearly unchanged (45.9 ± 3.2 versus 43.9 ± 2.6 in the controls). Further, after betamethasone treatment, a significant diminution (p<0.01) of the monoenic PC 32 species (palmitoyl- palmitoleyl PC and palmitoleyl-palmitoyl-PC) and the PC 34 species (consisting primarily of palmitoyl-oleoyl- PC) could be demonstrated both in absolute and relative terms. This is in agreement with a significant reduction of the portions of palmitoleic (p<0.01) and oleic (p<0.05) acids in the total PC fatty acids. The findings suggest two different mechanisms of DPPC elevation in fetal rat lungs for L-carnitine and betamethasone.