Arachidonic acid metabolism in galactosamine/endotoxin induced acute liver injury in rats.

The changes of the levels of LTC4, PGI2 and TXA2 in the liver tissue in SD rats with GaIN/LPS-induced acute liver injury was studied with radioimmunoassay (RIA). As a result, 12 h after the administration of GaIN/LPS, serum AST (398 +/- 37 u), ALT (565 +/- 43 u) increased (P < 0.001) and the concentration of TXA2 (12,188 +/- 588 pg/g.w.wt) in liver tissue increased significantly (P < 0.001), while the content of LTC4 (9713 +/- 3557 ng/g.w.wt) and PGI2(1748 +/- 560 pg/g.w.wt) in liver tissue were not obviously changed (P > 0.05) and the inflammatory changes of the pathological findings were observed. The improvement of serum ALT (330 +/- 168 u) (P < 0.05) and AST (273 +/- 124 u) (P < 0.05) and histopathological damage was observed after the administration of diethylcarbamazine (DEC), a LTA4 synthesis inhibitor, the liver TXA2 (12,740 +/- 699) concentration significantly increased (P < 0.001), while the levels of LTC4 (8179 +/- 1653) and PGI2 (2320 +/- 630) were not obviously changed. Serum ALT (536 +/- 74 u) and AST (416 +/- 41 u) (P > 0.05) levels and histopathology did not change with administration of indomethacin, a cyclooxygenase inhibitor, but the liver LTC4 (12,166 +/- 1327) contents increased (P < 0.05) and TXA2 (1868 +/- 791) reduced significantly (P < 0.001). The present study suggests that arachidonic acid metabolism in rats with acute liver injury are significantly abnormal. Leukotrienes and thromboxane are important inflammatory mediators in the liver injury.