Abstract
BackgroundDysregulation 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.AimTo develop a method for the assessment of 59Fe in residual tissue blood content and to correct this influence in 59Fe body distribution studies.MethodsIron 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 discussionThe 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.ConclusionsDifferences 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.Keywords: Iron-distribution; Mouse; Kinetics; Residual blood
Original language | English |
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Pages (from-to) | 19-32 |
Journal | Toxicology |
Volume | 241 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 2007 |