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内源性铁排泄。控制铁代谢的一种定量方法?

Endogenous iron excretion. A quantitative means to control iron metabolism?

作者信息

Kreuzer M, Kirchgessner M

机构信息

Institut für Ernährungsphysiologie, Technische Universität München-Weihenstephan, Freising, Germany.

出版信息

Biol Trace Elem Res. 1991 May;29(2):77-92. doi: 10.1007/BF03032686.

Abstract

The effects of supplemental oral (0, 40, and 400 ppm) and parenteral iron (0 and 2.72 mg Fe iv given initially as a single dose) on iron absorption, excretion, and retention were determined in 30 rats. Endogenous fecal iron excretion was determined by the radioisotope dilution technique after im injection of 80 kBq Fe-59, using blood and certain body tissues as reference sources for the estimation of the specific activity (Bq Fe-59/micrograms Fe) of endogenous iron. The basal diet contained 3.6 ppm Fe. Fe(III)-hydroxide-polymaltose was used as the sole iron source in oral, iv, and im iron treatments. Iron balance as determined from day 14 to 20 of the experiment was not significantly affected by iv iron administration. Nevertheless, a temporarily reduced retention should have occurred, since differences in final body iron contents were lower than 2.72 mg, as compared to the respective untreated groups. Apparent iron absorption and iron retention increased with surplus oral iron, and the efficiency rates were highest with adequate iron supply (40 ppm). True absorption rates of iron were similar without any, and with 40 ppm Fe amounting 40 to 50% of the intake. In the iron deficient rats, half of the actually absorbed iron (about 16 micrograms/d) was lost by endogenous fecal re-excretion, and another 3 micrograms/d by the urinary route. Endogenous loss with feces and with urine increased with further oral iron supply, but at a considerably lower rate as total fecal excretion. Parenterally administered iron did not affect endogenous loss at all. The results indicate that endogenous excretion cannot be regarded as a means to eliminate excessive iron, and might actually be an inevitable loss.

摘要

在30只大鼠中测定了补充口服铁(0、40和400 ppm)和胃肠外铁(0和2.72 mg铁,静脉注射,初始为单次剂量)对铁吸收、排泄和潴留的影响。通过放射性同位素稀释技术,在肌肉注射80 kBq铁-59后,以内源性铁的比活度(Bq铁-59/微克铁)估计,使用血液和某些身体组织作为参考来源,测定内源性粪便铁排泄。基础饮食含铁3.6 ppm。氢氧化铁-聚麦芽糖用作口服、静脉注射和肌肉注射铁治疗的唯一铁源。实验第14天至20天测定的铁平衡未受到静脉注射铁给药的显著影响。然而,由于与各自未治疗组相比,最终身体铁含量差异低于2.72 mg,因此应该出现了暂时的潴留减少。口服铁过量时,表观铁吸收和铁潴留增加,铁供应充足(40 ppm)时效率最高。铁的真实吸收率在无铁和含铁40 ppm时相似,占摄入量的40%至50%。在缺铁大鼠中,实际吸收的铁的一半(约16微克/天)通过内源性粪便再排泄丢失,另外3微克/天通过尿液途径丢失。随着口服铁供应增加,粪便和尿液中的内源性丢失增加,但速率远低于总粪便排泄。胃肠外给予铁根本不影响内源性丢失。结果表明,内源性排泄不能被视为消除过量铁的一种方式,实际上可能是一种不可避免的损失。

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