[14C]Arachidonic acid conversion in lung homogenates of 28-day fetuses from control and alloxan-diabetic rabbits was studied. The major metabolites were 12-l-hydroxy-5,8,10,14-eicosatetraenoic acid and prostaglandin E2. Small amounts of 6-ketoprostaglandin F1α prostaglandin F2α, and thromboxane B2 were also observed. Lung homogenates from fetuses of alloxan-diabetic rabbits convert significantly less [14C]arachidonic acid to prostaglandin E2, whereas all other metabolites were present in similar quantities compared to fetuses of non-diabetic rabbits. These studies suggest that the decreased arachidonic acid conversion to prostaglandin E2 could be partially responsible for the functional delay of lung maturation in offspring of alloxan-diabetic rabbits.
|Original language||English (US)|
|Number of pages||5|
|Journal||Biochimica et Biophysica Acta (BBA)/Lipids and Lipid Metabolism|
|State||Published - Aug 18 1982|
Bibliographical noteFunding Information:
The authors wish to thank Dr. Patrick Wong for his advice and help, and Brad Syverson, Barbara Jensen and Penny Bagne for their expert technical assistance. This study was supported in part by grants from the Juvenile Diabetes Foundation (79R139), the Minnesota Medical Foundation (DRF-3-78), the American Diabetes Association, Minnesota Affiliate, the Graduate School of the University of Minnesota (M.Y.T.), and NIH grant AM-16797 (D.M.B.).
- (Fetal rabbit lung)
- Prostaglandin metabolism
- Respiratory distress