On possible different mechanisms subserving the release of arachidonic and di-homo-gamma-linolenic acids for the formation of monoenoic and bisenoic prostaglandins in uteri from ovariectomized rats

Abstract

The uptake of arachidonic acid (AA) and of di-homo-gamma-linolenic acid (DGLA) and their incorporations into phospholipids (PLs) and into neutral lipids (NLs) of uteri isolated from spayed rats and the effect of inhibiting triglyceride (TG) metabolism with 4-pentenoic acid (4-PEA) on tissue TG levels and the output of prostaglandins (PGs), were explored. Attempts were also made to determine whether the acylation of labelled AA and of labelled DGLA into PLs and TGs is different and to confirm possible correlations between the synthesis of PGE 1 and the degradation of TGs. Uterine PLs incorporated significantly less DGLA than AA (P < 0.05). AA was acylated mainly into the phosphatidylinositol (PI) and into phosphatidylcholine (PC) subfractions of rat uteri, whereas the incorporation of DGLA into these two subfractions was significantly smaller than that of AA. The acylation of labelled DGLA into NL fractions, mainly into triacylglycerol, almost doubled that of labelled AA. The levels of TGs in isolated rat uteri suspended in glucose-free medium during a period of 60 minutes were significantly less than immediately after isolation (P < 0.001). PGE 1 released from uteri into the incubating solution, was significantly higher than that of PGE 2. Moreover, the presence of 4-PEA (1.0 mM), added after tissue isolation, prevented the decrement of TGs observed following 60 minutes of incubation and simultaneously diminished significantly (P < 0.001) the enhanced output of PGE 1, without altering that of PGE 2. Results presented herein suggest that PLs are not normal precursors for the synthesis of PGE 1. In addition, the present findings appear to support the notion that TGs and a triglyceride lipase are factors involved in the release of DGLA from storage sites to be used in the synthesis of monoenoic PGs. This situation appears different to that evoked by phospholipase A 2 inducing the release of AA from PLs and resulting in the generation of bisenoic PGs.