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Related Experiment Video

Updated: Jun 21, 2026

Measurement of Tissue Non-Heme Iron Content using a Bathophenanthroline-Based Colorimetric Assay

Measurement of Tissue Non-Heme Iron Content using a Bathophenanthroline-Based Colorimetric Assay

Published on: January 31, 2022

Hepcidin in acute iron toxicity.

Michal Toledano¹, Eran Kozer, Lee H Goldstein

¹Pharmacy Department, Assaf Harofeh Medical Center, Zerifin 70300, affiliated to the Sackler Faculty of Medicine, Tel Aviv University, Israel.

The American Journal of Emergency Medicine

|August 18, 2009

Summary

Acute iron poisoning in rats significantly increased liver hepcidin expression. This suggests hepcidin may play a role in the body's response to iron overload.

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Area of Science:

Biochemistry
Toxicology
Molecular Biology

Background:

Hepcidin is a key regulator of iron homeostasis, controlling iron release from macrophages and intestinal absorption.
Understanding hepcidin's role in acute iron poisoning is crucial for managing iron overload.

Purpose of the Study:

To investigate the expression of hepcidin in the liver during acute iron poisoning.
To establish a rat model for studying iron toxicity and hepcidin regulation.

Main Methods:

Male Wistar rats were administered a lethal dose (750 mg/kg) of elemental iron or distilled water (control).
Serum iron, liver transaminases (AST, ALT), and uric acid levels were measured.
Hepcidin messenger RNA (mRNA) levels were quantified in liver tissue.

Main Results:

Rats exposed to iron showed significantly elevated serum iron, AST, ALT, and uric acid levels compared to controls.
Hepcidin mRNA levels in the liver were significantly higher in the iron-intoxicated group (P = .005).

Conclusions:

Acute iron intoxication leads to a significant upregulation of hepcidin expression in the liver.
Further research is warranted to explore the correlation between hepcidin levels and the severity of iron intoxication.