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Effect of 13‐Hydroperoxyoctadecadienoic Acid on the Supply of Arachidonic Acid for Prostaglandin Synthesis from Arachidonoyl‐CoA Mediated by the Cytosolic or Microsomal acyl‐CoA Hydrolase in Rabbit Kidney Medulla

The effects of 13‐hydroperoxyoctadecadienoic acid (13‐HPODE) on the cytosolic or microsomal acyl‐CoA hydrolase (ACH) activity in rabbit kidney medulla and on the ACH‐mediated prostaglandin (PG) formation fromarachidonoyl‐CoA (AA‐CoA) were examined. 13‐HPODE (10, 20, and 50 mu M) had no effect on the cytosolic ACH activity but significantly inhibited the activity of the microsomal enzyme (43‐57% inhibition). PG formation was measured as follows: AA‐CoA (20 nmol) was preincubated with the cytosolic or microsomal fraction (as the source of ACH) in the presence or absence of 13‐HPODE for 5 min at 37° C, followed by incubation with the microsomal fraction (as the source of PG‐synthesizing enzymes), hydroquinone and reduced glutathione for 5 min at 37° C, and the PGs formed were measured by HPLC, with use of 9‐anthryldiazomethane for derivatization. 13‐HPODE reduced the PG formation when the microsomal fraction, but not the cytosolic fraction, was used as the source of ACH (10,20, and 50 mu M; 28‐55% inhibition). These results suggest that 13‐HPODE may modulate PG levels in rabbit kidney medulla by inhibiting the microsomal ACH activity.