We have previously shown that hydrogen peroxide (H2O 2) can inhibit K+-depolarization-evoked [ 3H]D-aspartate release from bovine isolated retinae. In the present study, we investigated the role of arachidonic acid metabolites in the inhibitory response elicited by H2O2 in the bovine retinae. Furthermore, we examined the direct effect of H2O 2 on the production of prostaglandins and isoprostanes in this tissue. Isolated bovine retinae were prepared for studies of [ 3H]D-aspartate release using the Superfusion Method. Release of [3H]D-aspartate was elicited by Krebs solution containing an iso-osmotic concentration of KCl (50 mM). A direct action of H2O 2 on prostaglandin E2 (PGE2) and 8-isoprostane F 2α (8-iso-PGF2α) was also measured by enzyme-linked immunosorbant assay (ELISA). The cyclooxygenase inhibitor, flurbiprofen (3 μM), or the thromboxane-receptor antagonist, SQ 29548 (10 μM) had no significant (p > 0.05) effect on K+-evoked [ 3H]D-aspartate release. On the other hand, both flurbiprofen (3 μM) and SQ 29548 (10 μM) blocked the inhibition of K+-evoked [3H]D-aspartate induced by H2O2 (30 μM). In concentrations up to 100 μM, H2O2 caused an increase in PGE2 and 8-iso-PGF2α over basal levels. For instance, H2O2 (100 μM) increased PGE2 and 8-iso-PGF2α over basal levels by 348 ± 41% and 185 ± 26 (n = 4), respectively. We conclude that the peroxide-mediated inhibition of [3H]D-aspartate may involve the production of prostaglandins and isoprostanes in the bovine isolated retinae.
All Science Journal Classification (ASJC) codes
- Sensory Systems
- Cellular and Molecular Neuroscience