Arachidonic acid metabolites and peroxide-induced inhibition of [3H]D-aspartate release from bovine isolated retinae.
Arachidonic acid metabolites and peroxide-induced inhibition of [3H]D-aspartate release from bovine isolated retinae.
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花生四烯酸代谢物和过氧化物诱导的对牛分离视网膜中[3H]D-天冬氨酸释放的抑制。
DOI：
10.1076/ceyr.28.5.367.28675
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发表时间：
2004
影响因子：
2
通讯作者：
Ohia,SunnyE
中科院分区：
文献类型：
--
作者：
LeDay,AngelaM;Kulkarni,KaustubhH;Opere,CatherineA;Ohia,SunnyE
我们之前已经证明过氧化氢（H 2 O 2）可以抑制K + -去极化引起的[ 3 H]D-天冬氨酸从牛离体视网膜中释放。在本研究中，我们研究了花生四烯酸代谢物在 H 2 O 2 引起的牛视网膜抑制反应中的作用。此外，我们还研究了 H 2 O 2 对该组织中前列腺素和异前列腺素产生的直接影响。制备分离的牛视网膜用于使用超融合法研究[ 3 H]D-天冬氨酸释放。 [ 3 H]D-天冬氨酸的释放由含有等渗浓度的 KCl (50mM) 的 Krebs 溶液引发。还通过酶联免疫吸附测定(ELISA)测量了H 2 O 2 对前列腺素E 2 (PGE2)和8-异前列腺素F 2a (8-iso-PGF 2a)的直接作用。环氧合酶抑制剂氟比洛芬 (3μM) 或血栓素受体拮抗剂 SQ 29548 (10μM) 对 K + 诱发的 [ 3 H]D-天冬氨酸释放没有显着影响 (p > 0.05)。另一方面，氟比洛芬 (3μM) 和 SQ 29548 (10μM) 均阻断 H 2 O 2 (30μM) 诱导的 K + 诱发的 [ 3 H]D-天冬氨酸的抑制作用。当浓度高达 100μM 时，H 2 O 2 导致 PGE 2 和 8-iso-PGF 2a 高于基础水平。例如，H 2 O 2 (100μM) 使 PGE 2 和 8-iso-PGF 2a 较基础水平分别增加 348 ± 41% 和 185 ± 26 (n = 4)。我们得出结论，过氧化物介导的[ 3 H]D-天冬氨酸抑制可能涉及牛离体视网膜中前列腺素和异前列腺素的产生。
We have previously shown that hydrogen peroxide (H 2 O 2) can inhibit K + -depolarization-evoked [ 3 H]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 H 2 O 2 in the bovine retinae. Furthermore, we examined the direct effect of H 2 O 2 on the production of prostaglandins and isoprostanes in this tissue. Isolated bovine retinae were prepared for studies of [ 3 H]D-aspartate release using the Superfusion Method. Release of [ 3 H]D-aspartate was elicited by Krebs solution containing an iso-osmotic concentration of KCl (50mM). A direct action of H 2 O 2 on prostaglandin E 2 (PGE2) and 8-isoprostane F 2a (8-iso-PGF 2a) was also measured by enzyme-linked immunosorbant assay (ELISA). The cyclooxygenase inhibitor, flurbiprofen (3µM), or the thromboxane-receptor antagonist, SQ 29548 (10µM) had no significant (p > 0.05) effect on K + -evoked [ 3 H]D-aspartate release. On the other hand, both flurbiprofen (3µM) and SQ 29548 (10µM) blocked the inhibition of K + -evoked [ 3 H]D-aspartate induced by H 2 O 2 (30µM). In concentrations up to 100µM, H 2 O 2 caused an increase in PGE 2 and 8-iso-PGF 2a over basal levels. For instance, H 2 O 2 (100µM) increased PGE 2 and 8-iso-PGF 2a over basal levels by 348 ± 41% and 185 ± 26 (n = 4), respectively. We conclude that the peroxide-mediated inhibition of [ 3 H]D-aspartate may involve the production of prostaglandins and isoprostanes in the bovine isolated retinae.