Apparent increases in phospholipid degradation and turnover during combined treatment with protein synthesis inhibitors and adrenocorticotropin

Inhibitors of protein synthesis, cycloheximide and puromycin, blocked ACTH (adrenocorticotropin)-induced increases in phospholipid mass, including phosphatidylinositol, but paradoxically increase ³²P-labelling (but not [³H]glycerol-labelling) therein. Cycloheximide also provoked an initial rapid decrease in ³²P-prelabelled phospholipids, followed by an increase in [³²P]P_i incorporation. These effects of cycloheximide and puromycin occurred in ACTH-treated (but not in control) cells. It appears that inhibition of protein synthesis during ACTH action provokes an increase in phospholipid degradation, followed by partial resynthesis of the phospholipid head groups.