Anemia of the Belgrade rat: evidence for defective membrane transport of iron

摘要: The mechanisms underlying the impaired utilization of transferrin-bound iron by erythroid cells in anemia Belgrade laboratory rat were investigated using reticulocytes from homozygous anemic animals and transferrin labeled with 59Fe 125I. results compared those obtained phenylhydrazine-treated rats iron-deficient rats. Each step uptake mechanism was investigated, ie, transferrin-receptor interaction, endocytosis, release transferrin, exocytosis. Although there quantitative differences, no fundamental difference found any abovementioned aspects cellular function when animals. basic defect must therefore reside subsequent steps uptake, after it is released within endocytotic vesicles, which transferred across lining membrane vesicles into cell cytosol. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) reticulocyte ghosts extracts demonstrated a prominent protein band mol wt 69,000 that absent or present only low concentration other two types reticulocytes. This may be result genetic defect.