Abstract
Intact liver could synthesize PGE 2, PGF 2α from arachidonic acid, whereas injured hepatocytes were able to synthesize TX in addition of PGE 2, PGF 2α. Normal liver homogenate could not produce TX from arachidonic acid because the supernatant fraction of the homogenate contained some inhibitor of TX biosynthesis. Intact hepatoma cells incorporated most of arachidonic acid into phospholipid, whereas hepatoma sonicate produced PGE 2, PGF 2α, TXB 2, 6-keto PGF 1α and 15-HPETE. The supernant fraction of hepatoma sonicate. did not contain the inhibitor of TX biosynthesis. Moreover, the supernatant fraction of hepatoma sonicate was able to synthesize PGE 2, PGF 2α, TXB 2 6-keto PGF 1α and 15-HPETE. Injured liver host temporarily the inhibitor of TX biosynthesis. TX with platelet-derived growth factor may collaborate to trigger pleiotypic responses in regenerating liver after partial hepatectomy.
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