Indicators of erythrocyte formation and degradation in rats with either vitamin A or iron deficiency

Vitamin A deficiency produces anemia and altered iron status. In this study with rats we rested two hypotheses regarding vitamin A deficiency: (1) tha t it impairs erythropoiesis, leading to an increased red cell turnover and (2) that it inhibits the glycosylation of transferrin. Erythropoietic activ ity was assessed indirectly, by determining the myeloid:erythroid ratio in bone marrow smears, the number of erythroid colonies in the red pulp of spl een, blood reticulocyte index, and zinc protoporphyrin and plasma transferr in receptor concentrations. Transferrin glycosylation was assessed by measu ring the sialic acid content of transferrin. The effects of vitamin A defic iency were compared with those of iron deficiency. Iron deficiency produced anemia and low iron levels in organs. Vitamin A deficiency produced low le vels of plasma and hepatic retinol, and it induced decreased plasma total i ron-binding capacity and raised iron levels in tibia and spleen. Short- but not long-term iron deficiency reduced the number oft erythroid colonies in spleen; vitamin A deficiency had no influence. Neither iron nor vitamin A deficiency influenced the myeloid:erythroid ratio in bone marrow smears and the blood reticulocyte production. Plasma transfer rin receptor and erythr ocyte zinc protoporphyrin concentrations Here not affected by vitamin A def iciency bur increased with iron deficiency. Vitamin A deficiency did not st imulate erythrocyte breakdown, as indicated by unaltered plasma lactate deh ydrogenase activity and reduced plasma total bilirubin levels. Both vitamin A and iron deficiencies raised the proportion of multiple sialylated trans ferrins in plasma. Thus, we have not found evidence that vitamin A deficien cy affects erythropoiesis and erythrocyte turnover The iron accumulation in spleen and bone marrow may be related to reduced iron transport due to inh ibition of transferrin synthesis rather than inhibition of transferrin sial ylation. (C) Elsevier Science Inc. 2000. All rights reserved.