Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development
Interactions between tissue uptake of lead and iron in normal and iron-deficient rats during development
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DOI：
10.1007/bf02789166
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发表时间：
1996-06-01
影响因子：
3.9
通讯作者：
Morgan, EH
中科院分区：
文献类型：
--
作者：
Crowe, A;Morgan, EH
环境铅中毒和缺铁是儿童常见的临床问题，常导致神经功能障碍。此外，已有研究表明，缺铁会增加肠道对铅的吸收。因此，有证据表明，铅和铁代谢之间的相互作用可能会导致大脑和其他组织对铅和铁的吸收发生变化。这些可能性是用15岁、21岁和63岁的大鼠进行的，这些大鼠的铁和铅营养状况不同。饲喂含0%或3%醋酸铅和0.2%醋酸铅的饲料。断奶后，饮用水中0.2%的醋酸铅成为日粮铅的唯一来源。在静脉注射转铁蛋白结合的Fe-59后，测量组织铅和非血红素铁的水平以及对Fe-59的摄取。膳食铅暴露大鼠的血液和肾脏铅水平表明，缺铁与肠道对铅的吸收增加有关。然而，缺铁并没有增加铅在脑中的沉积，所有大鼠的脑铅水平都相对较低(<；0.1mgg/g)。肝脏中的铅浓度低于2微克/克，而肾脏中的铅浓度几乎是这个浓度的20倍。与对照组相比，缺铁动物的肝脏铁水平较低，而大脑对Fe-59的摄取增加。然而，无论动物的铁状态如何，大脑和肾脏的铁水平都不会受到铅中毒的影响。铁-59的摄取率也不受铅的影响，但铁缺乏的大鼠的摄取率明显增加。铅确实提高了所有铁充足的大鼠的肝脏铁水平，但铁缺乏的影响很小。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，而且摄取铅的发生与动物的铁状况无关。此外，这项研究中产生的铅中毒水平并不影响大脑和肾脏对铁的吸收，但如果铁水平已经足够，肝脏铁的储备量可能会增加。
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. Darns 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 Fe-59 after intravenous injection of transferrin-bound Fe-59. 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 mu g/g). Lead concentrations in the liver were below 2 mu g/g, whereas kidneys had almost 20 times this concentration. Animals with iron deficiency had lower liver iron levels and had increased brain Fe-59 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. Fe-59 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 tl-lat 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.