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发育过程中正常和缺铁大鼠体内铅与铁的组织摄取之间的相互作用。

Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development.

作者信息

Crowe A, Morgan E H

机构信息

Department of Physiology, University of Western Australia, Perth.

出版信息

Biol Trace Elem Res. 1996 Jun;52(3):249-61. doi: 10.1007/BF02789166.

Abstract

Environmental lead intoxication, which frequently causes neurological disturbances, and iron deficiency are clinical problems commonly found in children. Also, iron deficiency has been shown to augment lead absorption from the intestine. Hence, there is evidence for an interaction between lead and iron metabolism which could produce changes in lead and iron uptake by the brain and other tissues. These possibilities were investigated using 15-, 21-, and 63-old rats with varying nutritional iron and lead status. Dams were fed diets containing 0 or 3% lead-acetate and 0.2% lead-acetate in the drinking water. After weaning, 0.2% lead-acetate in the drinking water became the sole source of dietary lead. Measurements were made of tissue lead and nonheme iron levels and the uptake of 59Fe after intravenous injection of transferrin-bound 59Fe. Iron deficiency was associated with increased intestinal absorption of lead as indicated by blood and kidney lead levels in rats exposed to dietary lead. However, iron deficiency did not increase lead deposition in the brain, and in all rats brain lead levels were relatively low (< 0.1 microgram/g). Lead concentrations in the liver were below 2 micrograms/g, whereas kidneys had almost 20 times this concentration. Animals with iron deficiency had lower liver iron levels and had increased brain 59Fe uptake in comparison to control rats. However, iron levels in brain and kidneys were unaffected by lead intoxication regardless of the animal's iron status. 59Fe uptake rates were also unaffected by lead, but increased rates of uptake were apparent in iron-deficient rats. Lead did increase liver iron levels in all iron-adequate rats, but iron deficiency had little effect. It is concluded that, compared with other tissues, the blood-brain barrier largely restricts lead uptake by the brain and that the uptake that does occur is unrelated to the iron status of the animal. Also, the level of lead intoxication produced in this investigation did not influence iron uptake by the brain and kidneys, but liver iron stores could be increased if iron levels were already adequate.

摘要

环境铅中毒常导致神经功能紊乱,缺铁是儿童常见的临床问题。此外,缺铁已被证明会增加肠道对铅的吸收。因此,有证据表明铅与铁代谢之间存在相互作用,这种相互作用可能会导致大脑和其他组织对铅和铁的摄取发生变化。我们使用15日龄、21日龄和63日龄且营养性铁和铅状态各异的大鼠对这些可能性进行了研究。给母鼠喂食含0%或3%醋酸铅的饲料,并在饮用水中添加0.2%醋酸铅。断奶后,饮用水中0.2%的醋酸铅成为膳食铅的唯一来源。我们测定了组织铅和非血红素铁水平,以及静脉注射转铁蛋白结合的59Fe后59Fe的摄取情况。缺铁与铅暴露大鼠血液和肾脏中的铅水平所表明的肠道对铅吸收增加有关。然而,缺铁并未增加大脑中的铅沉积,并且在所有大鼠中大脑铅水平相对较低(<0.1微克/克)。肝脏中的铅浓度低于2微克/克,而肾脏中的铅浓度几乎是其20倍。与对照大鼠相比,缺铁动物的肝脏铁水平较低,大脑对59Fe的摄取增加。然而,无论动物的铁状态如何,大脑和肾脏中的铁水平均不受铅中毒影响。59Fe摄取率也不受铅的影响,但缺铁大鼠的摄取率明显增加。在所有铁充足的大鼠中,铅确实会增加肝脏铁水平,但缺铁对此影响不大。得出的结论是,与其他组织相比,血脑屏障在很大程度上限制了大脑对铅的摄取,并且所发生的摄取与动物的铁状态无关。此外,本研究中产生的铅中毒水平并未影响大脑和肾脏对铁的摄取,但如果铁水平已经充足,肝脏铁储备可能会增加。

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