Figure 11
Schematic view of the results obtained after one or eight months of exposure to TAA, HTO and external irradiation and of the hypothesis possibly explaining the observed results. The hypothesis proposed is that local damages produced by TAA in the intestine induced a decreased ferritin expression which resulted in a decreased ability of iron transport through the intestinal barrier. As a result of insufficient iron availability, a decrease in RBC is observed and changes in iron metabolism in the spleen after one month of exposure. Due to both the persistent damage in the intestine with iron accumulation, this leads to iron deficit in the blood at 8 months. The increase in MVG thus appears as a compensation mechanism for the reduced number of RBC at one month. Hepcidin low concentration in the blood appears as a positive regulator of iron capture by the intestine at one month, not effective due to the persistent damage with the continuous presence of TAA. Such local damage is not induced by HTO or external irradiation due to the homogeneous distribution of radiation dose and damages.
