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Related Experiment Videos

ATP in iron overload-induced intracellular calcium changes

L J Anghileri1, P Thouvenot

  • 1Laboratory of Biophysics, Faculty of Medicine, University of Nancy, BP 184, F-54505 Vandoeuvre les Nancy, France.

International Journal of Molecular Medicine
|December 16, 1998
PubMed
Summary

Cellular iron uptake from complexes like ferric citrate depends on concentration, with ATP aiding translocation. Iron overload likely stems from inhibited Ca2+-ATPase activity, impairing calcium extrusion.

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Area of Science:

  • Cellular Biology
  • Biochemistry
  • Toxicology

Background:

  • Cellular iron uptake mechanisms are crucial for various biological processes.
  • Dysregulation of iron homeostasis can lead to cellular damage and pathologies.
  • Understanding iron complex interactions with cells is vital for disease research.

Purpose of the Study:

  • To investigate the cellular uptake of low molecular weight iron complexes.
  • To elucidate the role of ATP and cellular proteins in iron handling.
  • To determine the mechanisms behind iron-induced calcium overload.

Main Methods:

  • Experiments using ferric citrate, ferric lactate, and ferric ATP complex.
  • Deferoxamine treatment to assess cellular iron penetration.

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  • Measurement of cellular Ca2+-uptake and CaATPase activity.
  • Evaluation of calcium channel blockers' effects.

    • Main Results:

    • Cellular iron uptake is concentration-dependent and largely limited.
    • ATP facilitates iron translocation, enhancing iron complex effects.
    • Cellular proteins act as a buffer against iron overload.
    • Iron complex concentration inhibits CaATPase activity, impairing calcium extrusion and causing overload.
    • Calcium channel blockers do not affect iron complex-cell interactions.

    Conclusions:

    • Cellular iron uptake from specific complexes is regulated and limited.
    • ATP plays a significant role in cellular iron translocation.
    • Inhibition of CaATPase activity is the primary cause of calcium overload induced by iron complexes, relevant to iron overload pathologies.