Tissue Iron Content
Tissue Iron Content - Related Videos
05:08
Measurement of Tissue Non-Heme Iron Content using a Bathophenanthroline-Based Colorimetric Assay
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Cited by 8 •
2022
Here, a protocol for the measurement of the non-heme iron content in animal tissues is provided, using a simple, well-established colorimetric assay that can be easily implemented in most laboratories.
07:12
A Colorimetric Method for Measuring Iron Content in Plants
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Cited by 3 •
2018
We present a simple and reliable protocol for measuring iron content in plant tissues using the colorimetric Prussian Blue method.
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.
03:03
Bathophenanthroline Sulfonate-Based Colorimetric Assay: A Simple and Rapid Method for Quantitation of Non-Heme Iron in Mouse Liver Tissue
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2025
In this video, we describe a colorimetric-based method to determine non-heme iron content in mouse liver tissue. Bathophenanthroline sulfonate is used as the chromogenic substrate in the presence of a reducing agent, which converts ferric iron to chelatable ferrous iron.
05:09
Soluble Protein Assay to Quantify Soluble Protein Content in Plant Tissues
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2025
This video describes a colorimetric method to quantify the soluble protein content in plant tissues. The method uses Coomassie Brilliant Blue G-250 dye, which interacts with the soluble protein to form a blue-colored stable protein-dye complex, proportional to the soluble protein content in the tissue.
FAQs
Iron movement depends on coordinated transport, uptake, storage, and export. Transferrin carries circulating iron to cells, where transferrin receptors support cellular uptake. Ferritin stores iron in a safer form, while ferroportin exports iron from cells. Together, these components influence whether iron remains available for cellular needs or accumulates within tissues.
Hepcidin regulates cellular iron release by binding ferroportin, the principal protein responsible for iron export. This interaction can alter how much iron leaves cells and therefore affects tissue retention. Because tissue accumulation may contribute to toxicity and organ injury, the hepcidin-ferroportin relationship is central to understanding disrupted iron balance.
Tissue iron measurements help distinguish several clinically important patterns of disrupted iron balance. They can support evaluation of iron deficiency, chronic inflammation, hereditary iron overload, and transfusion-related overload. Interpreting the result in that clinical context is important because abnormal tissue iron may reflect inadequate availability, altered regulation, excessive storage, or potential injury.
The liver, heart, and endocrine tissues receive particular attention because iron accumulation in these sites can have important clinical consequences. Assessments in these organs help identify where abnormal storage or potential toxicity is occurring. This organ-focused information supports diagnosis and helps clinicians monitor whether iron-related disease is affecting vulnerable tissues.
These assessments contribute to diagnosing abnormal iron balance and monitoring treatment over time. They are relevant when clinicians investigate deficiency, chronic inflammation, hereditary iron overload, or iron accumulation associated with transfusions. Results can also help indicate whether iron dysregulation is associated with organ injury, particularly in the liver, heart, or endocrine tissues.
Tissue iron measurements support research into how disrupted iron homeostasis contributes to disease progression. Investigators can examine relationships among abnormal storage, anemia, oxidative stress, and injury in specific organs. This context helps connect molecular regulation by transferrin, ferritin, hepcidin, and ferroportin with clinically observable consequences of iron imbalance.