由海藻酸盐损伤的培养视网膜神经元中钙依赖性自由基的产生

Calcium-dependent free radical generation in cultured retinal neurons injured by kainate.

作者信息

Dutrait N, Culcasi M, Cazevieille C, Pietri S, Tordo P, Bonne C, Muller A

机构信息

Laboratoire de Physiologie Cellulaire, Université Montpellier, France.

出版信息

Neurosci Lett. 1995 Sep 22;198(1):13-6. doi: 10.1016/0304-3940(95)11948-v.

DOI:10.1016/0304-3940(95)11948-v

PMID:8570085

Abstract

Cultured rat retinal neurons exposed to kainate produced free radicals, as demonstrated by electron spin resonance (ESR) spin trapping using the nitrone 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and the generation of DMPO hydroxyl adduct (DMPO-OH). This DMPO-OH production was abolished by EGTA, nitro-arginine and oxypurinol, suggesting that it was dependent on Ca2+ influx and subsequent activation of nitric oxide synthase and xanthine oxidase. Moreover, kainate induced a receptor-mediated Ca2+ influx and neuronal injury assessed by lactate dehydrogenase release. Neuroprotection afforded by nitro-arginine and oxypurinol shows that calcium-dependent free radical production plays a major role in kainate retinal toxicity.

摘要

使用硝酮5,5-二甲基-1-吡咯啉-N-氧化物（DMPO）的电子自旋共振（ESR）自旋捕获以及DMPO羟基加合物（DMPO-OH）的生成证明，暴露于红藻氨酸的培养大鼠视网膜神经元会产生自由基。EGTA、硝基精氨酸和氧嘌呤醇可消除这种DMPO-OH的产生，这表明它依赖于Ca2+内流以及随后一氧化氮合酶和黄嘌呤氧化酶的激活。此外，红藻氨酸诱导了受体介导的Ca2+内流以及通过乳酸脱氢酶释放评估的神经元损伤。硝基精氨酸和氧嘌呤醇提供的神经保护作用表明，钙依赖性自由基产生在红藻氨酸视网膜毒性中起主要作用。