ironuptake

Iron uptake refers to the acquisition of iron from the environment by living organisms. Iron is essential for respiration, DNA synthesis, and metabolism, but its bioavailability is limited by low solubility and tight regulation. Consequently, different groups have evolved strategies to extract iron from ferric (Fe3+) or ferrous (Fe2+) forms and to transport it to cells while avoiding iron-induced toxicity.

In humans and other vertebrates, dietary iron is absorbed primarily in the duodenum and proximal jejunum. Non-heme iron (Fe3+) is reduced to Fe2+ by brush-border ferrireductases and transported into enterocytes by DMT1. Fe2+ may be stored in ferritin or exported via ferroportin on the basolateral membrane; iron is oxidized to Fe3+ by hephaestin or ceruloplasmin and bound to transferrin in plasma. Heme iron uses specific uptake pathways and is released intracellularly by heme oxygenase. Systemic iron homeostasis is influenced by hepcidin, a liver-derived hormone that binds ferroportin and limits iron efflux during inflammation or iron overload.

In plants, two main uptake strategies exist. Non-grass species (strategy I) acidify the rhizosphere, reduce Fe3+ to Fe2+ with ferric-chelate reductase (FRO2), and take up Fe2+ through IRT1. Grasses (strategy II) secrete phytosiderophores that chelate Fe3+ and import the complexes via specific transporters such as YS1/YS3; these are complemented by other transporters and ferritin storage.

Bacteria employ siderophores—high-affinity iron-binding molecules—to scavenge iron from the environment. The iron-siderophore complex is recognized by outer-membrane receptors and transported into the cell through energy-providing systems such as TonB-ExbB-ExbD, with iron released by intracellular enzymes and stored in ferritin or utilized in metabolic processes.