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Oxidative pathways in the sickle cell and beyond.

Abdu I Alayash1

  • 1Laboratory of Biochemistry and Vascular Biology, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, USA.

Blood Cells, Molecules & Diseases
|May 31, 2017
PubMed
Summary

Sickle cell disease involves red blood cell polymerization and oxidative damage. This review explores how microparticles, free hemoglobin, and heme contribute to vascular issues and discusses new antioxidant therapies.

Keywords:
Ferryl hemoglobinHeme oxidationMicroparticlesPseudoperoxidaseSickle cell hemoglobin

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Area of Science:

  • Hematology
  • Molecular Biology
  • Vascular Biology

Background:

  • Sickle cell disease (SCD) is characterized by deoxy sickle hemoglobin (HbS) polymerization, leading to red blood cell (RBC) sickling.
  • RBCs in SCD face oxidative stress, increasing hemolysis and contributing to vasculopathy.
  • Vaso-occlusive crises elevate RBC-derived microparticles and extracellular hemoglobin (Hb) in circulation.

Purpose of the Study:

  • To provide insights into the interplay between microparticles, free Hb, and heme in sickle cell disease.
  • To focus on Hb's pseudoperoxidative activity and its role in RBC damage and vascular oxidative toxicity.
  • To discuss emerging antioxidative strategies for managing Hb oxidative pathways.

Main Methods:

  • Review of existing literature on HbS polymerization, oxidative stress, microparticles, and heme in SCD.
  • Analysis of the mechanisms by which free Hb and heme contribute to cellular and vascular damage.
  • Exploration of the pseudoperoxidative activity of Hb.

Main Results:

  • Heme, a byproduct of Hb oxidation and from Hb-laden microparticles, acts as a damage-associated molecular pattern (DAMP) molecule, initiating inflammation.
  • Hb's pseudoperoxidative activity drives changes in RBC cytosol and membranes, leading to oxidative toxicity.
  • Microparticles, free Hb, and heme collectively contribute to the vasculopathy observed in sickle cell disease.

Conclusions:

  • The interaction between microparticles, free Hb, and heme is a critical factor in SCD pathogenesis.
  • Hb's oxidative activity is a key driver of RBC damage and vascular complications.
  • Antioxidative strategies targeting protein and heme scavenging show promise in mitigating Hb-driven oxidative pathways.