Biomedical Research on Trace Elements
Online ISSN : 1880-1404
Print ISSN : 0916-717X
ISSN-L : 0916-717X
吉田 宗弘山川 裕久湯川 法子野口 伸之助福永 健治西山 利正
ジャーナル フリー

2013 年 24 巻 1 号 p. 23-30


In patients with a renal failure, control of the absorption of dietary phosphate is necessary to prevent hyperphosphataemia. Recently, it has been proposed that ferric citrate is used as a phosphate-binder for patients with renal failure. However, several recent studies have indicated that an accumulation of iron in liver causes cirrhosis and liver cancer. In the present study, we examined iron accumulation in tissues of rats administered a large amount of ferric citrate.
Male 4-week-old Wistar rats were fed AIN93G diet (basal diet) or the basal diet supplemented with 1.0 or 4.0% ferric citrate hydrate (FCH; iron content, 18.5%) for 4 weeks. Administration of 4.0% FCH significantly inhibited the rat growth. However, liver function and lipid metabolism were not influenced by the FCH administration. Fecal phosphorus excretion was dose-dependently increased by the FCH administration and serum phosphate was significantly lower in the 4% FCH group compared to the other two groups. Serum iron and transferrin saturation was dose-dependently increased by the FCH administration. In particular, transferrin saturation of the 4.0% FCH group was near 100%. Iron in the liver, kidney, spleen and femur were markedly increased by the FCH administration; in particular, the increase of the hepatic iron was proportional to the dietary iron concentration. In addition, hemosiderin was accumulated in the cytoplasm of liver. These results indicate that transferrin is saturated and siderosis is caused by oral administration of a large amount of ferric citrate.

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