Iron overload of spleen, liver and kidney as a consequence of hemolytic anaemia

Iron overload in spleen, liver and kidney induced by hemolytic anaemia due to a 90-day oral exposure of rats to diuron (N-3,4-dichlorphenyl-N,N-dimethylurea), an urea herbicide, was studied by histochemistry, transmission electronmicroscopy, morphometry and energy dispersive X-ray microanalysis. Increasing dosages of diuron provoked a hemosiderosis in the spleen followed by erythrocytic sequestration and the formation of haemopoietic foci coinciding with Kupffer cell siderosis of the liver. A strong enlargement of the spleen red pulp on the one hand faces an unchanged total white pulp volume as well as no alterations of the white pulp microscopic structure on the other. The electron dense bodies of the endothelial cells did not contain iron whereas hepatocytes possess two types of lysosomes, homogeneous iron containing ones at the sinusoidal site and complex structured ones without detectable iron at the biliary site. The formation of the homogeneous lysosomes is suggested to be due to the hepatocytic reception of hemoglobin-haptoglobin-complexes after intravascular hemolysis. The lysosomes of the biliary site seem to be engaged in hemoglobin degradation. A partial nephrohydrosis due to hemosiderotic events in succession of intravascular hemolysis including hemoglobin reabsorption from the primary urine could be observed. It is assumed that exocytosis might play a major role in hemosiderin removal from kidney tubule cells.