Young rapidly-growing weanling rats accumulate ferritin iron in the liver; riboflavin deficiency inhibits this process and is associated with reduced in vitro iron-mobilising activity at the gastro-intestinal mucosa. Adult rats that are not growing tend to maintain existing stores of iron. Whereas riboflavin deficiency reduces in vitro iron-mobilising activity at the gastro-intestinal mucosa, this has no impact on body iron stores in these animals. Levels of circulating iron, on the other hand, are significantly reduced, possibly due to some interference with iron release from the reticuloendothelial system. The magnitude of the impact of riboflavin deficiency on iron mobilisation from body stores and iron absorption may depend upon a number of factors, likely to include the size of existing hepatic iron stores and the demand for rapid iron turnover.