IRON SUPPLEMENTATION MODERATES BUT DOES NOT CURE THE BELGRADE ANEMIA

Belgrade rats inherit microcytic, hypochromic anemia as an autosomal r ecessive trait (gene symbol b), Erythrocytes and tissue are iron defic ient in the face of elevated TIBC (total iron binding capacity) and pe rcent iron saturation; iron injections increased the number of erythro cytes but their appearance remained abnormal. We have investigated iro n supplements to improve husbandry of b/b rats and to learn more about the underlying defect and its tissue distribution, Weekly IM (intramu scular) injections of iron-dextran (Imferon at 30 mg kg(-1)) improved the anemia but did not alter the red cell morphology. Certain diets al so improved the health of b/b rats when compared to standard rat chows by the criteria of weight, survival to adulthood, hematology and repr oduction, The critical nutritional factor turned out to be iron bioava ilability, with ferrous iron added to the diet improving the health of Belgrade rats without affecting the underlying erythroid defect, Tiss ue iron measurements after dietary or parenteral supplementation confi rmed the iron deficient status of untreated b/b rats and established t hat dietary ferrous iron partially relieved this deficiency, with inje ctions leading to greater amounts of tissue iron, Serum iron and TIBC were also found to be elevated in untreated b/b rats, with dietary sup plementation decreasing but not eliminating the elevation in TIBC, The se studies indicate that iron supplements can improve the health of b/ b rats without altering the underlying defect and also suggest that th e mutation could alter iron uptake in the GI (gastrointestinal) tract.