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缺铁的小鼠和人类受试者对膳食镉的吸收增加。

Increased dietary cadmium absorption in mice and human subjects with iron deficiency.

作者信息

Flanagan P R, McLellan J S, Haist J, Cherian G, Chamberlain M J, Valberg L S

出版信息

Gastroenterology. 1978 May;74(5 Pt 1):841-6.

PMID:640339
Abstract

In mice fed a low iron diet, the addition of low levels of cadmium chloride (10 micrometer) to the drinking water impaired growth and accentuated the development of anemia. Cadmium had no effect on mice given a similar diet supplemented with iron. Iron deficiency increased the concentration of cadmium in the duodenal mucosa, the transfer of cadmium to the body from the intestinal tract, and the deposition of absorbed cadmium in the kidneys. In human subjects, the average absorption of 25 microgram of cadmium, labeled with 115mCd, from a test meal was 8.9 +/- 2.0% (mean +/- SE) in 10 people with low body iron stores (serum ferritin less than 20 ng per ml) and 2.3 +/- 0.3% in 12 subjects with normal iron stores (serum ferritin greater than 23 ng per ml). The biological half-time of the radiocadmium in 3 of the subjects ranged from 90 to 202 days. Thus, the intestinal adaptive response to iron deficiency in both experimental animals and human subjects leads to the increased absorption of cadmium, a potentially toxic element.

摘要

在喂食低铁饮食的小鼠中,向饮用水中添加低水平的氯化镉(10 微摩尔)会损害生长并加重贫血的发展。镉对喂食补充了铁的类似饮食的小鼠没有影响。缺铁会增加十二指肠黏膜中镉的浓度、镉从肠道向体内的转移以及吸收的镉在肾脏中的沉积。在人类受试者中,10 名体内铁储备低(血清铁蛋白低于 20 纳克/毫升)的人从一顿测试餐中平均吸收 25 微克用 115mCd 标记的镉的吸收率为 8.9±2.0%(平均值±标准误),而 12 名铁储备正常(血清铁蛋白大于 23 纳克/毫升)的受试者的吸收率为 2.3±0.3%。3 名受试者中放射性镉的生物半衰期在 90 至 202 天之间。因此,实验动物和人类受试者对缺铁的肠道适应性反应都会导致镉这种潜在有毒元素的吸收增加。

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