Iron Metabolism
Iron Metabolism - Related Videos
08:45
Quantitating Iron Transport Across the Mouse Placenta In Vivo Using Nonradioactive Iron Isotopes
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Cited by 3 •
2022
This article demonstrates how to prepare and administer transferrin-bound nonradioactive isotopic iron for studies of iron transport in mouse pregnancy. The approach for quantifying isotopic iron in fetoplacental compartments is also described.
03:06
Culturing Mycobacterium tuberculosis Under Iron-Limited Conditions
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2025
Source: Gupta, S., et al. Isolation and Characterization of Extracellular Vesicles Produced by Iron-limited Mycobacteria. J. Vis. Exp. (2019)This video demonstrates the procedure for culturing Mycobacterium tuberculosis under iron-limited conditions to induce iron stress and promote the secretion of siderophores that support bacterial survival.
00:52
What is Metabolism?
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2019
Overview Metabolism represents all of the chemical activity in a cell, including reactions that build molecules (anabolism) and those that break molecules down (catabolism). Anabolic reactions require energy, whereas catabolic reactions provide it. Thus, metabolism describes how cells transform energy through a variety of chemical reactions, which are often made more efficient with the help of enzymes. Metabolism Is the Sum of All of the Chemical Reactions That Take Place in an Organism
05:41
Metabolic Profile Analysis of Zebrafish Embryos
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Cited by 42 •
2013
Zebrafish represent a powerful vertebrate model that has been under-utilised for metabolic studies. Here we describe a rapid way to measure the in vivo metabolic profile of developing zebrafish that allows the comparison of different mitochondrial function parameters between genetically or pharmacologically manipulated embryos, thereby increasing the applicability of this organism.
06:37
Staphylococcus aureus Growth using Human Hemoglobin as an Iron Source
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Cited by 31 •
2013
Here we describe a growth assay for Staphylococcus aureus using hemoglobin as the sole source of available nutrient iron. This assay establishes the role of bacterial factors involved in hemoglobin-derived iron acquisition.
FAQs
Hepcidin–ferroportin signaling adjusts whether iron leaves cells and enters circulation. Ferroportin provides the export route, while hepcidin controls that route according to body demand. This regulation helps coordinate intestinal iron entry with the need to supply hemoglobin synthesis and iron-containing enzymes, while limiting unregulated iron availability that could contribute to oxidative damage.
Transferrin mainly carries circulating iron in the bloodstream, providing a controlled delivery system for tissues that require it. Ferritin stores iron inside cells, creating a reserve while reducing exposure to excess free iron. Together, transport and storage separate iron distribution from longer-term retention, supporting cellular use without leaving large amounts unbound.
Iron supports essential functions, including oxygen transport and cellular energy production, but excess free iron can promote oxidative damage. Iron metabolism therefore balances availability with sequestration in storage forms such as ferritin and regulated export through the hepcidin–ferroportin pathway. This balance allows iron-dependent processes to continue while limiting potentially harmful unrestrained iron.
Disruption can produce too little usable iron for hemoglobin synthesis or excessive iron accumulation in the body. These opposing outcomes reflect failures in the network that coordinates absorption, transport, storage, recycling, and release. Examining the pathway helps connect altered iron handling with anemia and overload, rather than treating either condition as an isolated transport problem.
A useful investigation follows iron through its major handling stages: entry into intestinal cells, circulation bound mainly to transferrin, storage in ferritin, cellular use, recycling, and regulated release. Tracking these stages helps researchers identify where iron availability changes and how the hepcidin–ferroportin pathway influences distribution according to overall body demand.
Iron metabolism provides a biological context for studying host–pathogen interactions because iron is both a controlled cellular resource and an essential element for oxygen transport and energy-related processes. Investigators can therefore examine how iron handling intersects with infection-related biology, alongside broader questions about iron distribution, storage, and the consequences of altered availability.
Studying the coordinated iron-handling network can clarify why iron balance changes in anemia and iron overload. The hepcidin–ferroportin pathway is especially relevant because it links body demand with iron export. This mechanistic understanding can guide investigation of potential diagnostic or treatment targets while preserving the iron needed for hemoglobin and cellular enzymes.