Effects of CO2 exposure on distribution of various forms of iron and copper in guinea-pig tissues

Summary The effects on iron and copper distribution and metabolism of exposure to high levels of CO₂ were studied in the guinea-pig. Mature, male animals were placed in an atmosphere of 15% CO₂, 21% O₂ (balance N₂), and sacrificed from 1 h to 1 week thereafter. Total iron and copper concentrations of blood, liver, spleen and bone, as well as concentrations of heme and ferritin iron, were measured together with blood hematocrit, reticulocytes, plasma hemoglobin, plasma ceruloplasmin and copper concentrations. The results show clearly that rapid and sustained red cell damage or hemolysis ensued several h from the start of CO₂ treatment. This resulted in loss of iron and copper from the blood, an influx of both elements into liver, spleen and bone, and a rise in plasma ceruloplasmin. Influx of iron into liver and spleen caused an accumulation of ferritin, the main site for iron storage in cells. Following the effect on red cells, there was an accumulation of heme iron, and a decreased hematocrit, best explained by a depressed activity of the reticuloendothelial and erythropoietic systems. A period of adaptation succeeded these events, in which all blood parameters and most tissue values returned to normal, despite the continuing presence of high CO₂. The only changes not reversed were the elevations in liver, spleen and bone iron stores. These remained high, with a net accumulation of >2 mg iron, or 3–4 times more than originally present. The results indicate that at least in the guinea-pig, high CO₂ exposure results in red cell damage and other events leading to an accumulation of additional iron in the body; also, that iron accumulated as ferritin and hemosiderin in liver and spleen may not be readily available to restore blood hemoglobin concentrations on an acute basis.Acknowledgments. We gratefully acknowledge the technical assistance of Joan R. Moor and Lakshmi Vulimiri with these studies, and the support of Grants No. 17249 and HL22410 from the U.S. Public Health Service.