Nikša Pokrajac

Incorporation of 32P into phospholipids in vivo during compensatory renal growth

Incorporation of 32P into phospholipids, RNA and DNA was studied in adult male C57BL/GoZgb mice. Left nephrectomy was performed under diethyl ether anesthesia, and the remaining right kidney was excised 10 min to 28 days later. Sham-operated animals were used as controls. 2 h before killing, animals were injected intraperitoneally with 37 kBq (1 microCi) 32P (as sodium orthophosphate) per g of body weight. In the right kidney, incorporation of 32P into total phospholipids, and five phospholipid fractions (phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, diphosphatidylglycerol and sphingomyelin) was increased by 25-35% between 20 and 72 h after uninephrectomy. The incorporation of 32P into RNA showed a similar pattern. However, incorporation of 32P into phosphatidylinositol and phosphatidic acid was already increased 20 min after uninephrectomy, reached a peak about 110-120% above control values 4 h after uninephrectomy, and then slowly returned to the control value at about 84-96 h. These results indicate that an early alteration in phospholipid metabolism, particularly of inositol lipids, may play a role in initiation of compensatory renal growth.

Plasma from Uninephrectomized Rats Increases 32P Incorporation into Phospholipids of Renal Cortical Slices

Incorporation of 32P into phospholipids of renal cortical slices was studied in vitro after addition of plasma from uninephrectomized or sham-operated rats. Plasma from uninephrectomized rats increased the labeling of phospholipids when obtained within the first hour after uninephrectomy. With different amounts of added plasma a graded response in labeling of phosphatidic acid and phosphatidylinositol was obtained. Phosphatidylcholine labeling also showed a graded response but only if the incubation was prolonged. The results suggest that an early alteration in phospholipid metabolism, particularly of inositol lipids, may play a role in initiation of compensatory renal growth by humoral factor(s).