Characterization of hydroxyl radical generation in the striatum of free-moving rats due to carbon monoxide poisoning, as determined by in vivo microdialysis
Characterization of hydroxyl radical generation in the striatum of free-moving rats due to carbon monoxide poisoning, as determined by in vivo microdialysis
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DOI：
10.1016/j.brainres.2004.05.047
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发表时间：
2004-08-06
期刊：
影响因子：
2.9
通讯作者：
Endo, T
中科院分区：
文献类型：
--
作者：
Hara, S;Mukai, T;Endo, T
一氧化碳（CO）中毒引起的CO暴露在3000 ppm的40分钟，导致刺激羟基自由基（circleOH）的产生（估计通过测量2，3-二羟基苯甲酸（2，3-DHBA）生产水杨酸）在自由活动的大鼠的纹状体，通过脑微透析测定。用电压依赖性Na+通道阻断剂河豚毒素（TTX）预处理，降低了2，3-DHBA的基础水平，并强烈抑制了CO中毒引起的2，3-DHBA的增加。一氧化碳中毒显着，虽然只是轻微，增加细胞外谷氨酸在纹状体，谷氨酸（Glu）受体拮抗剂，如MK-801（地佐环平）和NBQX，。未能抑制CO诱导的2，3-DHBA增加。这些结果表明，CO中毒可能通过电压依赖性Na+通道诱导Na+内流，导致刺激大鼠纹状体circleOH的产生。这种效应可能不依赖于细胞外Glu增加对Glu受体的激活。(C)2004 Elsevier B. V.保留所有权利。
Carbon monoxide (CO) poisoning caused by CO exposure at 3000 ppm for 40 min resulted in stimulation of hydroxyl radical (circleOH) generation (estimated by measuring 2,3-dihydroxybenzoic acid (2,3-DHBA) production from salicylic acid) in the striatum of free-moving rats, as determined by means of brain microdialysis. Pretreatment with a voltage-dependent Na+ channel blocker, tetrodotoxin (TTX), lowered the basal level of 2,3-DHBA and strongly suppressed the increase in 2,3-DHBA induced by CO poisoning. CO poisoning significantly, though only slightly, increased extracellular glutamate in the striatum, and glutamate (Glu) receptor antagonists, such as MK-801 (dizocilpine) and NBQX,. failed to suppress the CO-induced increase in 2,3-DHBA. These findings suggest that CO poisoning may induce Na+ influx via the voltage-dependent Na+ channels, resulting in stimulation of circleOH generation in rat striatum. This effect may be independent of Glu receptor activation by increased extracellular Glu. (C) 2004 Elsevier B.V. All rights reserved.