PubMed · 4449028
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W F Stanaszek, R S Levinson, B Ecanow. 1974. Halothane uptake by coacervate systems.. https://doi.org/10.1002/jps.2600631225
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The absorption of 137Cs by sheep following ingestion of contaminated soil was studied using an established dual isotope method. Two agricultural soils were studied: an alluvial gley contaminated by discharges to the sea from the Sellafield Reprocessing Plant, and a lowland organic soil that had been artificially contaminated. Values of the true absorption coefficient of radiocaesium of 0.19 +/- 0.03 and 0.03 +/- 0.01, respectively, were obtained for these soils. This implies that availability of soil-associated radiocaesium for uptake following ingestion is up to about 20% of that when the activity is incorporated in vegetation. These results have been compared to estimates of availability made using an in-vitro approach described previously and found to be in good agreement. However, comparison with in-vitro data obtained for an upland peat indicated that absorption from some upland organic soils could be greater than from the lowland organic soil.
Previously, hepatic iron overload resembling that in hereditary hemachromatosis (HH) has been found in beta 2-microglobulin knockout (beta 2m-/-) mice. We have now characterized iron metabolism in beta 2m-/- mice. The mutant mice fail to limit the transfer of iron from mucosal cells into the plasma. Transferrin saturation is abnormally high. Pathologic iron depositions occur predominantly in liver parenchymal cells. Reconstitution with normal hematopoietic cells redistributes the iron from parenchymal to Kupffer cells, but does not correct the mucosal defect. We conclude that (a) iron metabolism is defective in the gut mucosa as well as the liver of beta 2m-/- mice; and (b) a beta 2m-dependent gene product is involved in iron homeostasis. Recently, a novel gene of the major histocompatibility complex class I family, HLA-H, has been found to be mutated in a large proportion of HH patients. Our data provide functional support for the proposed causative role of HLA-H mutations in HH.
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