Arachidonic acid metabolites and peroxide-induced inhibition of [ 3H]D-aspartate release from bovine isolated retinae

Angela M. LeDay, Kaustubh H. Kulkarni, Catherine A. Opere, Sunny E. Ohia

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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 (8-iso-PGF) 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-PGF over basal levels. For instance, H2O2 (100 μM) increased PGE2 and 8-iso-PGF 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.

Original languageEnglish
Pages (from-to)367-372
Number of pages6
JournalCurrent Eye Research
Volume28
Issue number5
DOIs
StatePublished - May 2004

Fingerprint

D-Aspartic Acid
Peroxides
Arachidonic Acid
Retina
Dinoprost
Dinoprostone
Flurbiprofen
Isoprostanes
8-epi-prostaglandin F2alpha
Prostaglandins
Thromboxane Receptors
Cyclooxygenase Inhibitors
Hydrogen Peroxide
Enzymes

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Sensory Systems

Cite this

Arachidonic acid metabolites and peroxide-induced inhibition of [ 3H]D-aspartate release from bovine isolated retinae. / LeDay, Angela M.; Kulkarni, Kaustubh H.; Opere, Catherine A.; Ohia, Sunny E.

In: Current Eye Research, Vol. 28, No. 5, 05.2004, p. 367-372.

Research output: Contribution to journalArticle

@article{2cfa07acaf5b49d798b1d34f5ba76233,
title = "Arachidonic acid metabolites and peroxide-induced inhibition of [ 3H]D-aspartate release from bovine isolated retinae",
abstract = "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.",
author = "LeDay, {Angela M.} and Kulkarni, {Kaustubh H.} and Opere, {Catherine A.} and Ohia, {Sunny E.}",
year = "2004",
month = "5",
doi = "10.1076/ceyr.28.5.367.28675",
language = "English",
volume = "28",
pages = "367--372",
journal = "Current Eye Research",
issn = "0271-3683",
publisher = "Informa Healthcare",
number = "5",

}

TY - JOUR

T1 - Arachidonic acid metabolites and peroxide-induced inhibition of [ 3H]D-aspartate release from bovine isolated retinae

AU - LeDay, Angela M.

AU - Kulkarni, Kaustubh H.

AU - Opere, Catherine A.

AU - Ohia, Sunny E.

PY - 2004/5

Y1 - 2004/5

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=2442453772&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2442453772&partnerID=8YFLogxK

U2 - 10.1076/ceyr.28.5.367.28675

DO - 10.1076/ceyr.28.5.367.28675

M3 - Article

VL - 28

SP - 367

EP - 372

JO - Current Eye Research

JF - Current Eye Research

SN - 0271-3683

IS - 5

ER -