title: Iron supplementation moderates but does not cure the Belgrade anemia.
abstract: Belgrade rats inherit microcytic, hypochromic anemia as an autosomal recessive trait (gene symbol b). Erythrocytes and tissue are iron deficient in the face of elevated TIBC (total iron binding capacity) and percent iron saturation; iron injections increased the number of erythrocytes but their appearance remained abnormal. We have investigated iron supplements to improve husbandry of b/b rats and to learn more about the underlying defect and its tissue distribution. Weekly i.m. (intramuscular) injections of iron-dextran (Imferon at 30 mg kg-1) improved the anemia but did not alter the red cell morphology. Certain diets also improved the health of b/b rats when compared to standard rat chows by the criteria of weight, survival to adulthood, hematology and reproduction. The critical nutritional factor turned out to be iron bioavailability, with ferrous iron added to the diet improving the health of Belgrade rats without affecting the underlying erythroid defect. Tissue iron measurements after dietary or parenteral supplementation confirmed the iron deficient status of untreated b/b rats and established that dietary ferrous iron partially relieved this deficiency, with injections leading to greater amounts of tissue iron. Serum iron and TIBC were also found to be elevated in untreated b/b rats, with dietary supplementation decreasing but not eliminating the elevation in TIBC. These studies indicate that iron supplements can improve the health of b/b rats without altering the underlying defect and also suggest that the mutation could alter iron uptake in the GI (gastrointestinal) tract.
authors.affiliation: Department of Biochemistry, SUNY, Buffalo 14214-3000, USA. mgarrick@ubmed.buffalo.edu
authors.forename: M
authors.initials: M
authors.lastname: Garrick
authors.forename: D
authors.initials: D
authors.lastname: Scott
authors.forename: S
authors.initials: S
authors.lastname: Walpole
authors.forename: E
authors.initials: E
authors.lastname: Finkelstein
authors.forename: J
authors.initials: J
authors.lastname: Whitbred
authors.forename: S
authors.initials: S
authors.lastname: Chopra
authors.forename: L
authors.initials: L
authors.lastname: Trivikram
authors.forename: D
authors.initials: D
authors.lastname: Mayes
authors.forename: D
authors.initials: D
authors.lastname: Rhodes
authors.forename: K
authors.initials: K
authors.lastname: Cabbagestalk
authors.forename: R
authors.initials: R
authors.lastname: Oklu
authors.forename: A
authors.initials: A
authors.lastname: Sadiq
authors.forename: B
authors.initials: B
authors.lastname: Mascia
authors.forename: J
authors.initials: J
authors.lastname: Hoke
authors.forename: L
authors.initials: L
authors.lastname: Garrick
mesh_terms: D000747:Anemia, Hypochromic / Q000178:diet therapy* / Q000235:genetics; D000818:Animals; D001682:Biological Availability; D048429:Cell Size / Q000187:drug effects; D004912:Erythrocytes / Q000166:cytology / Q000187:drug effects; D005260:Female; D005527:Food, Fortified; D006397:Hematinics / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D006454:Hemoglobins / Q000378:metabolism; D007273:Injections, Intramuscular; D007408:Intestinal Absorption / Q000235:genetics; D007501:Iron / Q000097:blood / Q000378:metabolism; D000090463:Iron Deficiencies; D019266:Iron, Dietary / Q000008:administration & dosage / Q000627:therapeutic use*; D007505:Iron-Dextran Complex / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D009154:Mutation / Q000235:genetics; D051381:Rats; D014018:Tissue Distribution
chemical_list: D006397:Hematinics; D006454:Hemoglobins; D019266:Iron, Dietary; D007505:Iron-Dextran Complex; D007501:Iron