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Lifecycle of Erythrocytes

Erythrocytes, also known as red blood cells, constantly move through blood capillaries. As a result, they damage their plasma membrane due to the continuous friction. Typically, after 100 to 120 days, erythrocytes become rigid and fragile as they wear out. As they pass through small vessels in the spleen and liver, they can get trapped and break apart into fragments.
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Related Experiment Video

Updated: Jun 4, 2026

Measurement of Heme Synthesis Levels in Mammalian Cells
09:43

Measurement of Heme Synthesis Levels in Mammalian Cells

Published on: July 9, 2015

Hemin Recapitulates the Labile Iron Pool in the Cellular Fenton Reaction with DNA.

Aaron M Fleming1, Cynthia J Burrows1

  • 1Department of Chemistry, University of Utah, 315 S 1400 E, Salt Lake City, Utah 84112-0850, United States.

Chemical Research in Toxicology
|June 3, 2026
PubMed
Summary

Physiological bicarbonate redirects the iron-Fenton reaction to form carbonate radical anion (CO3•−), not hydroxyl radical. Heme iron is identified as the likely driver of this DNA-damaging reaction in cells.

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Electrophoretic Mobility Shift Assay (EMSA) for the Study of RNA-Protein Interactions: The IRE/IRP Example

Published on: December 3, 2014

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oxidative Stress Research

Background:

  • The iron-Fenton reaction is central to biological redox processes, with hydroxyl radical (HO•) or ferryl species (Fe=O2+) traditionally considered the primary oxidants.
  • Recent findings suggest physiological bicarbonate can redirect this reaction, favoring the formation of carbonate radical anion (CO3•−) over HO•/Fe=O2+.
  • Uncertainty remains regarding the influence of oxygen (O2) concentration, ascorbate, and specific iron speciation on CO3•− generation.

Purpose of the Study:

  • To investigate the roles of O2 concentration, ascorbate, and iron speciation in bicarbonate-dependent carbonate radical anion (CO3•−) formation during the iron-Fenton reaction.
  • To monitor bicarbonate-mediated telomeric DNA damage in cellulo under physiological conditions.
  • To identify the specific iron species responsible for CO3•− production in a cellular context.

Main Methods:

  • In cellulo studies were performed using cell cultures under physiological O2 levels (∼25 μM) with ascorbate replenishment to assess bicarbonate-dependent telomeric DNA damage.
  • In vitro plasmid nicking assays were conducted using cellular low molecular weight (LMW) ultrafiltrate under controlled O2, bicarbonate, and hydrogen peroxide (H2O2) concentrations.
  • A panel of iron complexes (hexaaquo-ferrous ion, ferrous citrate, ferrous α-ketoglutarate, ferrous pyrophosphate, ferrous glutathione, and hemin) were tested in vitro and in a defined biomimetic metabolome.

Main Results:

  • Under physiological conditions, 25 mM bicarbonate promoted 2'-deoxyguanosine-specific oxidation, consistent with CO3•− formation, at a ratio exceeding 80:1 compared to HO•/Fe=O2+.
  • In vitro experiments mirrored cell culture results, showing exclusive CO3•− formation with LMW ultrafiltrate under physiological O2, bicarbonate, and 500 nM H2O2.
  • Only hemin among the tested iron complexes reproduced the bicarbonate-dependent CO3•− damage profile observed in cells, even at lower H2O2 concentrations (100 nM).

Conclusions:

  • Heme iron is identified as a key species capable of driving the bicarbonate-mediated iron-Fenton reaction to produce carbonate radical anion (CO3•−).
  • This pathway leads to specific damage at 2'-deoxyguanosine residues in DNA during endogenous oxidative stress.
  • The findings highlight the critical role of iron speciation, particularly heme iron, in determining the nature of oxidants generated during biological redox reactions.