A method to assess ⁵⁹Fe in residual tissue blood content in mice and its use to correct ⁵⁹Fe-distribution kinetics accordingly

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• 作者：Klaus Schü ; mann ; Bernadett Szegner ; Birgit Kohler ; Michael W. Pfaffl ; Thomas Ettle
• 关键词：Iron-distribution ; Mouse ; Kinetics ; Residual blood
• 刊名：Toxicology
• 出版年：2007
• 出版时间：20 November 2007
• 年：2007
• 卷：241
• 期：1-2
• 页码：19-32
• 全文大小：649 K

文摘

Background

Dysregulation of body iron-distribution may induce oxidative damage. To investigate the molecular mechanisms of iron homeostasis, corresponding essential genes are manipulated by many working groups. This asks for a simple method to pursue the resulting impact on body iron-distribution in mice.

Aim

To develop a method for the assessment of ⁵⁹Fe in residual tissue blood content and to correct this influence in ⁵⁹Fe body distribution studies.

Methods

Iron status in male adult C57BL6 mice was adjusted by feeding diets with different iron content. Fractional contribution of organs to total body weight was determined after dissection. ⁵⁹Fe-labelled blood was injected in recipient mice to estimate total blood volume and residual blood content in all organs and tissues. The main experiment used these data to correct total ⁵⁹Fe tissue content at six intervals after ⁵⁹Fe injection (12 h–28 days).

Results and discussion

The sum of ⁵⁹Fe in all organs was the same as determined in each mouse before dissection. ⁵⁹Fe in whole blood remained constant from the 4th day after injection on, and was highest in iron-deficiency. As in other species, residual blood content was highest in spleen and lungs. Nevertheless, ⁵⁹Fe in the iron-deficient spleen decreased to zero and intestinal ⁵⁹Fe-content also decreased significantly over time after correction for ⁵⁹Fe in residual blood. These findings suggest correct assessment of compartment sizes and ⁵⁹Fe in residual blood in each organ.

Conclusions

Differences in ⁵⁹Fe-distribution between iron status reflected changes in the expression of proteins of iron-transport and its regulation correctly. Thus, the method seems suitable to analyse body iron-distribution in consequence to genetic manipulations of murine iron homeostasis which is a prerequisite to assess possible toxicological consequences of iron supplementation.