Development of hemolytic anemia in rats fed selenite

Abstract

The anemia of selenite toxicity in rats was studied with 59Fe. When the 59Fe was injected into control animals and into selenite-fed animals which would soon show anemia, the uptake of radioactivity in the blood was the same. In observing the fatal anemia that then developed with the selenite-fed animal, an extensive decline of the hemoglobin concentration and of the newly incorporated 59Fe in the blood occurred at the same time. An interruption of the decline might occur. At death, the overall reduction of the hemoglobin concentration in the blood was less than the reduction of the label. During the terminal stage, hemoglobinuria occurred. The animals which did not show extensive loss of the 59Fe in the blood also did not show anemia or die. The results indicated that the anemia was caused by hemolysis rather than by a defect in red blood cell synthesis. The effect of the selenite treatment on the 59Fe loss from the blood was reduced when arsenite was included in the diet. The use of arsenite in the diet without selenite also appeared to have some sparing effect on the 59Fe loss. When arsenite was fed with labeled selenite, a reduction in the selenium level in the liver and kidneys occurred. Thus, arsenite addition to a selenite-treated diet was associated with a reduction in hemolysis and in selenium accumulation in certain organs.