al-Deeb S, al-Moutaery K, Bruyn G W, Tariq M
Research Center, Armed Forces Hospital, Riyadh, Saudi Arabia.
J Psychiatry Neurosci. 1995 May;20(3):189-92.
The present investigation was undertaken to study the effect of selenium on experimental dyskinesia in rats. The movement disorders were produced in rats by intraperitoneal administration of iminodipropionitrile (IDPN) in the dose of 100 mg/kg per day for 12 days. Selenious acid was administered daily 30 minutes before IDPN in the doses of 5 mumol/kg, 10 mumol/kg and 20 mumol/kg bodyweight in three different groups of rats. Animals were observed daily for any neurobehavioral changes including circling, backwalking, head weaving and twitching. Immediately after behavioral studies, blood and brain specimens were collected for analysis of thiobarbituric acid reactive substances (TBARS) to measure the extent of free radical production. Our results showed that concurrent use of selenium significantly inhibited IDPN-induced neurobehavioral changes in a dose-dependent manner. Treatment of rats with selenium also reduced the TBARS production in blood and different regions of brain. These findings suggest that selenium attenuates the IDPN-induced neurotoxicity by inhibiting lipid peroxidation.
本研究旨在探讨硒对大鼠实验性运动障碍的影响。通过每天腹腔注射100 mg/kg的亚氨基二丙腈(IDPN),连续注射12天,诱导大鼠出现运动障碍。在三组不同的大鼠中,分别在每天注射IDPN前30分钟,以5 μmol/kg、10 μmol/kg和20 μmol/kg体重的剂量给予亚硒酸。每天观察动物的任何神经行为变化,包括转圈、倒退行走、头部摆动和抽搐。行为学研究结束后,立即采集血液和脑标本,分析硫代巴比妥酸反应物质(TBARS),以测量自由基产生的程度。我们的结果表明,同时使用硒能以剂量依赖的方式显著抑制IDPN诱导的神经行为变化。用硒处理大鼠还降低了血液和脑不同区域的TBARS生成。这些发现表明,硒通过抑制脂质过氧化减轻了IDPN诱导的神经毒性。