实验性应激诱导大鼠不同组织微量元素水平的变化

Yunus Karakoc, Ertan Yurdakos, Tevfik Gulyasar, Murat Mengi, U. Bora Barutcu
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引用次数: 18

摘要

在本研究中,我们研究了急性和慢性固定应激对大鼠颞叶、脑干、脾脏和肝组织锌、铜和铁水平的影响。急性应激组动物置于笼中,一次仅120分钟。对于慢性应激组(2小时和4小时),大鼠每天分别在笼中饲养2和4小时,连续5天。将对照组和固定大鼠斩首,然后采集组织样本。用火焰原子吸收分光光度计测定颞叶、脑干、脾脏和肝脏中的Zn、Cu和Fe水平。我们的研究结果表明,急性固定化应激会导致脑组织内源性锌和铜的释放。在2小时慢性应激组中,颞叶和脑干的Fe水平显著升高,而脾脏和肝脏的Fe水平降低。在4小时慢性应激组中,颞叶和脑干的Fe水平增加,而脾脏和肝脏的Zn和Cu水平增加。在急性和慢性固定应激组中,锌和铜的动员可能与肝和脾中金属硫蛋白(MT)的诱导有关,但与脑中的诱导无关。另一方面,颞叶和脑干中过量的铁使我们相信,大脑铁转运蛋白可能参与并增强了固定应激。J.Trace Elem。Exp.Med.16:55-602003。©2003 Wiley-Liss,股份有限公司。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Experimental stress-induced changes in trace element levels of various tissues in rats
In this study, we investigated the effects of acute and chronic immobilization stress on the Zn, Cu, and Fe levels of the temporal lobe, brain stem, spleen, and liver tissues in rats. The animals in the acute stress group were put in the cages, one time only for 120 min. For the chronic stress groups (2h and 4h), the rats were kept in the cages daily for 2 and 4 h, respectively, for 5 consecutive days. Controls and immobilized rats were decapitated, and then tissue samples were taken. Zn, Cu, and Fe levels in the temporal lobe, brain stem, spleen, and liver were measured by flame atomic absorption spectrophotometer. Our results showed that acute immobilization stress causes endogenous Zn and Cu release from the brain tissues. In the 2h chronic stress group, Fe levels markedly increase in the temporal lobe and brain stem whereas they decrease in the spleen and liver. In the 4h chronic stress group, Fe levels increase in the temporal lobe and brain stem while Zn and Cu levels increase in the spleen and liver. In the acute and chronic immobilization stress groups, mobilization of Zn and Cu can be related to the induction of metallothionein (MT) in the liver and spleen but not in the brain. On the other hand, excess Fe in the temporal lobe and brain stem causes us to believe think that the brain iron transport proteins may be involved, and enhanced, by immobilization stress. J. Trace Elem. Exp. Med. 16:55–60, 2003. © 2003 Wiley-Liss, Inc.
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