Hepatic erythropoietin production in the lead-poisoned rat.

A NEMIA OF VARIOUS degrees of severity occurs following lead poisoning. This anemia is usually hypochromic with an increased reticulocyte count and increased red cell hemolysis. These changes are attributed to an inhibition of several enzymes involved in heme synthesis, an interference with the transport ofiron, as well as changes in the erythrocyte membrane.1 A defect in erythroid differentiation and maturation has also been noted.2 Lead poisoning also results in renal tubular dysfunction, and characteristic intranuclear inclusion bodies are found in the tubular lining cells of rats.3 The importance of functioning renal tissue for the regulation of normal erythropoiesis by the production or activation of the hormone erythropoietin is well established, as is the finding that extrarenal erythropoietin production occurs.4 Evidence will be presented that in the lead-poisoned rat (1) extrarenal erythropoietin production is increased, and (2) the liver is necessary for extrarenal erythropoietin production to occur.