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镉在未接触镉的正常大鼠、缺铁大鼠以及镉诱导的缺铁动物体内的潴留情况。

Retention of cadmium in cadmium-naive normal and iron-deficient rats as well as in cadmium-induced iron-deficient animals.

作者信息

Schäfer S G, Schwegler U, Schümann K

机构信息

Kali-Chemi AG, Department of Non-Clinical Safety Evaluation, Hannover, Federal Republic of Germany.

出版信息

Ecotoxicol Environ Saf. 1990 Aug;20(1):71-81. doi: 10.1016/0147-6513(90)90047-9.

Abstract

The retention of cadmium was investigated in cadmium-naive normal and iron-deficient rats in comparison to rats with cadmium-induced iron deficiency. Rats subchronically (4 weeks) exposed to dietary cadmium (28, 56, 112 ppm Cd and 28 ppm Fe) received a radioactively labeled dose of 2 mumol Cd/kg body wt; acutely (no cadmium exposure with diet) treated rats received doses between 1 and 8 mumol Cd/kg body wt. Two animals of each group received iron (1 mumol/kg as 59FeSO4 in order to monitor iron absorption in parallel. After a period of 4 weeks of feeding a cadmium-fortified diet, the test dose was administered and after a 2-weeks period 109Cd and of 59Fe retention was determined. The results showed in part an unexpected pattern of cadmium retention: subchronic feeding of cadmium induced iron deficiency. This implies an immediate interaction between the two metals with regard to intestinal transfer of iron. The retention of iron was increased in the Cd-induced anemia to the same extent as that in iron deficiency induced by iron restriction. Cadmium retention in iron deficiency induced by iron withdrawal also showed a marked increase, which implies that iron deficiency stimulates the intestinal transfer system for both metals in a similar way. Contrary to this effect, the cadmium retention in cadmium-induced iron deficiency was reduced to about 30% of control values. A self-induced aggravation of the body cadmium burden, as a consequence of the iron deficiency which is known to result from subchronic exposure to feeding of dietary cadmium, was thus excluded.

摘要

在未接触过镉的正常大鼠和缺铁大鼠中,研究了镉的潴留情况,并与镉诱导缺铁的大鼠进行了比较。将大鼠亚慢性(4周)暴露于膳食镉(28、56、112 ppm镉和28 ppm铁)中,给予放射性标记剂量的2 μmol镉/千克体重;急性处理(饮食中无镉暴露)的大鼠接受1至8 μmol镉/千克体重的剂量。每组两只动物接受铁(1 μmol/千克,以59FeSO4形式,以便同时监测铁的吸收)。在喂食含镉强化饮食4周后,给予测试剂量,2周后测定109Cd和59Fe的潴留情况。结果部分显示出意外的镉潴留模式:亚慢性喂食镉会导致缺铁。这意味着两种金属在铁的肠道转运方面存在直接相互作用。镉诱导的贫血中铁的潴留增加程度与铁限制诱导的缺铁相同。铁缺乏导致的缺铁中镉的潴留也显著增加,这意味着缺铁以类似方式刺激两种金属的肠道转运系统。与这种效应相反,镉诱导缺铁中的镉潴留减少至对照值的约30%。因此排除了由于亚慢性暴露于膳食镉喂养导致的缺铁而引起的机体镉负担的自我加重。

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