Phenols inhibit prostaglandin E2 synthesis in A23187-stimulated human whole blood and modify the ratio of arachidonic acid metabolites.

We have previously demonstrated that the phenolic compounds catechol, hydroquinone, and phenol increase the prostaglandin (PG) E2/leukotriene (LT) B4 ratio in human polymorphonuclear leukocytes (PMNs), while resorcinol has the opposite effect. However, in human whole blood phenols have a different effect on the thromboxane (TX) B2/LT ratio than in PMNs on the PGE2/LTB4 ratio. To establish whether the discrepancy between the results of our previous studies is due to different indicators of prostaglandin H synthase activity in PMNs (PGE2) and in whole blood (TXB2), we measured the effect of phenols on PGE2 synthesis in whole blood. The phenols only inhibited PGE2 synthesis (IC50 values for resorcinol, catechol, hydroquinone, and phenol of 10 microM, 10 microM, 60 microM and 700 microM, respectively). No significant stimulatory activity was seen as earlier in PMNs. Thus, the effect of phenols on PGE2 synthesis in whole blood is different from that in PMNs, although their order of potency to inhibit PGE2 synthesis is the same.