クエン酸第二鉄を長期間経口投与した成熟ラットのトランスフェリン飽和率と肝臓への鉄蓄積

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  • Transferrin Saturation and Hepatic Iron Deposition in Mature Rats with Long-term Oral Exposure to Ferric Citrate
  • クエンサン ダイニテツ オ チョウキカン ケイコウ トウヨ シタ セイジュク ラット ノ トランスフェリン ホウワリツ ト カンゾウ エ ノ テツ チクセキ

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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, tissue iron deposition and serum transferrin saturation were examined in mature rats with long-term oral exposure to high dose of ferric citrate. Male 10-week old Wistar rats were fed AIN93M diet (basal diet) or the basal diet supplemented with 1.0% or 4.0% ferric citrate hydrate (FCH; iron content, 18.5%) for 24 weeks. Administration of FCH increased fecal phosphorus excretion dose-dependently. However, serum phosphorus concentrations in the FCH-exposed rats were not lower than those in the rats without exposure to FCH. Iron contents in the serum, liver, kidney and femur as well as transferrin saturation of rats fed the 4.0% FCH diet increased with the progress of feeding period and were significantly higher than those of the other rats. In particular, the hepatic iron deposition levels were increased to 3.3, 4.7 and 13.4 times higher than those in the rats without FCH exposure at the 4th, 12th and 24th week, respectively. Iron deposition levels in the spleen were dose-dependently increased by the FCH-exposure but saturated at the 12th week. Hemosiderin accumulation was observed in the liver cytoplasm of rats fed the 4.0% FCH rats and increased with progress of the exposure period. These results indicate that both of tissue iron deposition and increase of transferrin saturation occur when the iron exposure exceeds a threshold value; ferric citrate should be used as a phosphate-binder only in the case where the increase in transferrin saturation does not occur.

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