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Iron speciation study in Hfe knockout mice tissues: magnetic and ultrastructural characterisation
Lucía Gutiérrez1, Carmen Quintana, Cristina Patiño
1Departamento de Ciencia y Tecnología de Materiales y Fluidos, Universidad de Zaragoza, Centro Politécnico Superior, c/ María de Luna, 3, 50018 Zaragoza, Spain. lucia@unizar.es
Biochimica Et Biophysica Acta
|April 8, 2009
Summary
Iron accumulation in DBA/2 Hfe knockout mice primarily affects the liver, with spleen and heart tissues showing no significant differences. This study characterizes iron speciation in a murine model of iron overload diseases.
Area of Science:
- Biophysics
- Materials Science
- Biochemistry
Background:
- Iron overload diseases are a group of disorders characterized by excessive iron accumulation.
- DBA/2 Hfe knockout mice serve as a murine model to study hereditary hemochromatosis, a type of iron overload disease.
- Understanding iron speciation is crucial for diagnosing and treating iron overload.
Purpose of the Study:
- To investigate the chemical iron speciation in liver, spleen, and heart tissues of DBA/2 Hfe knockout mice.
- To characterize ferritin-like species and other iron deposits using magnetic susceptibility measurements and electron microscopy.
- To differentiate iron accumulation in hepatic tissue from spleen and heart tissues.
Main Methods:
- Low temperature AC magnetic susceptibility measurements.
- Transmission Electron Microscopy (TEM).
- Selected Area Electron Diffraction.
Main Results:
- Iron accumulation was primarily observed in the hepatic tissue of knockout mice.
- Spleen and heart tissues showed no significant differences between knockout and wild-type animals.
- TEM revealed diverse iron deposits including ferritins, siderosomes, haematite, and goethite in hepatocytes and extracellular spaces.
Conclusions:
- DBA/2 Hfe knockout mice model demonstrates significant iron accumulation in the liver.
- Magnetic susceptibility and TEM provide complementary insights into iron speciation and distribution.
- The findings contribute to understanding the pathophysiology of iron overload diseases.
