Crowe A, Morgan E H
Department of Physiology, University of Western Australia, Nedlands, Perth.
Toxicol Appl Pharmacol. 1997 Jul;145(1):136-46. doi: 10.1006/taap.1997.8165.
Little is known regarding the interactions between iron and cadmium during postnatal development. This study examined the effect of altered levels of dietary iron and cadmium loading on the distribution of cadmium and iron in developing rats ages 15, 21, and 63 days. The uptake of iron, transferrin, and cadmium into various organs was also examined using 59Fe, [125I]transferrin, and 109Cd. Dietary cadmium loading reduced packed cell volume and plasma iron and nonheme iron levels in the liver and kidneys, evidence of the inducement of an iron deficient state. Dietary iron loading was able to reverse these effects, suggesting that they were the result of impaired intestinal absorption of iron. Cadmium loading resulted in cadmium concentrations in the liver and kidneys up to 20 microg/g in rats age 63 days, while cadmium levels in the brain reached only 0.16 microg/g, indicating that the blood-brain barrier restricts the entry of cadmium into the brain. Iron loading had little effect on cadmium levels in the organs and cadmium feeding did not lower tissue iron levels in iron loaded animals. These results suggest that cadmium inhibits iron absorption only at low to normal levels of dietary iron and that at high levels of intake iron and cadmium are largely absorbed by other, noncompetitive mechanisms. It was shown that 109Cd is removed from the plasma extremely quickly irrespective of iron status and deposits mainly in the liver. One of the most striking effects of cadmium loading on iron metabolism was increased uptake of [125I]transferrin by the heart, possibly by disrupting the process of receptor-mediated endocytosis and recycling of transferrin by heart muscle.
关于出生后发育过程中铁与镉之间的相互作用，人们了解甚少。本研究考察了饮食中铁水平的改变以及镉负荷对15日龄、21日龄和63日龄发育中大鼠体内镉和铁分布的影响。还使用59Fe、[125I]转铁蛋白和109Cd检测了铁、转铁蛋白和镉在各个器官中的摄取情况。饮食中镉负荷降低了红细胞压积以及肝脏和肾脏中的血浆铁和非血红素铁水平，这是铁缺乏状态被诱导的证据。饮食中铁负荷能够逆转这些影响，表明它们是铁肠道吸收受损的结果。镉负荷导致63日龄大鼠肝脏和肾脏中的镉浓度高达20微克/克，而大脑中的镉水平仅达到0.16微克/克，这表明血脑屏障限制了镉进入大脑。铁负荷对器官中的镉水平影响很小，而给铁负荷动物喂食镉并不会降低组织铁水平。这些结果表明，镉仅在饮食中铁处于低至正常水平时抑制铁吸收，而在高摄入量时，铁和镉主要通过其他非竞争性机制被吸收。结果表明，无论铁状态如何，109Cd都能极快地从血浆中清除，并且主要沉积在肝脏中。镉负荷对铁代谢最显著的影响之一是心脏对[125I]转铁蛋白的摄取增加，这可能是通过破坏受体介导的内吞作用以及心肌中转铁蛋白的再循环过程实现的。
