turpentine-induced hyperplastic bone marrow, and chlo roma tumor to transform precursor arachidonic acid into prostaglandmns. The activity of the prostaglandin synthetase

Data from our present studies demonstrate the capability of a 105,000 x g pellet from rat normal bone marrow, turpentine-induced hyperplastic bone marrow, and chlo roma tumor to transform precursor arachidonic acid into prostaglandmns. The activity of the prostaglandin synthetase systems in these tissues is inhibited by the known nonster oid antiinflammatory drug indomethacin and by two unsat urated fatty acids previously demonstrated in other tissues. Although the overall biosynthesis of prostaglandin E, (PGE2)was higher in the hyperplastic bone marrow than in the chloroma tumor, the PGF2Q:PGE2ratio was markedly higher (8-fold) in the chloroma tissue. This latter increase was probably due to the increased transformation of PGE2 into PGF2Qby the NADPH-dependent PGE29-ketoreductase (an enzyme that catalyzes the transformation of PGE2and PGF20).These results indicate the greater capability of the malignant chloroma tissue to form PGF20than of nonmalig nant hyperplastic bone marrow. Although the role of PGF20 in the malignant myelogenous leukemic tumor is presently unclear, its increased formation in this tissue suggests that this substance may play a role in the hyperproliferative process.