Changes in serum hepcidin levels in acute iron intoxication in a rat model

Toxicol Lett. 2009 Sep 28;189(3):242-7. doi: 10.1016/j.toxlet.2009.06.848. Epub 2009 Jun 12.

Abstract

Hepcidin is an important and recently discovered regulator of iron homeostasis. Acute iron intoxication is one of the leading causes of overdose mortality in children. It is difficult to estimate the degree of iron intoxication since iron serum levels do not correlate with the actual clinical severity. In the current study we aimed to investigate whether serum hepcidin levels are elevated in acute iron intoxication. Rats were divided into two iron dose groups and one control group. Each group was further subdivided into four time groups following the administration of iron. Levels of hepcidin, iron and liver enzymes were measured, and animals were followed for signs of toxicity. Serum hepcidin levels were significantly higher in the group treated with toxic doses of iron (p=0.005). No significant difference in serum iron levels was found between the groups. In acute iron intoxication serum hepcidin levels increase significantly and remain elevated for at least 6h. We postulate that beyond the first hour after iron administration, serum hepcidin levels provide a better estimate of the amount of iron intake than do serum iron levels.

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Antimicrobial Cationic Peptides / blood*
  • Aspartate Aminotransferases / blood
  • Dose-Response Relationship, Drug
  • Enzyme-Linked Immunosorbent Assay
  • Ferrous Compounds / toxicity
  • Hepcidins
  • Intestines / pathology
  • Iron / toxicity*
  • Iron Overload / blood*
  • Liver / drug effects
  • Liver / enzymology
  • Liver / pathology
  • Male
  • Rats
  • Rats, Wistar
  • Uric Acid / metabolism

Substances

  • Antimicrobial Cationic Peptides
  • Ferrous Compounds
  • Hamp protein, rat
  • Hepcidins
  • Uric Acid
  • ferrous sulfate
  • Iron
  • Aspartate Aminotransferases
  • Alanine Transaminase