Abstract
The mechanism by which utilization of transferrin-bound iron is linked with cellular metabolism has been studied in isolated rat hepatocytes. The initial binding of transferrin to the hepatocyte is not dependent on metabolic energy, but the subsequent progressive binding of transferrin and uptake of iron depend on metabolic energy and the drainage of reducing equivalents from the respiratory chain. When respiration is completely blocked with cyanide a limiting energy level for the uptake of iron is found at an intracellular concentration of ATP of approximately 0.2 mmol/1. The iron uptake process utilizes ATP hydrolysis, substrate oxidation and dissipation of ionic gradients as energy sources interchangeably.