ABSTRACT
This chapter deals with research performed which has considerably increased the understanding of the mechanisms involved in the translational regulation of ferritin mRNA availability in order to achieve iron homeostasis. Injection of iron salts into the peritoneal cavity of the rat is quickly followed by the synthesis of extra ferritin subunits by a mechanism that is not quenched by prior injection of actinomycin D. This mechanism is unlikely to involve transcription but rather translation. The interpretation was strengthened when a large stock of dormant mRNAs of ferritin H and L subunits were identified in the cell sap of rats untreated with iron. Factors other than iron can alter the expression of ferritin genes, usually differentially favoring the H subunit. Tin-mesoporphyrin, an inhibitor of heme breakdown by the oxygenase, delayed the induction of ferritin. The iron-responsive element motif performs a different function in regulating the stability of the transferrin receptor in response to changes in the intracellular iron level.
