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Iron toxicity - Its effect on the bone marrow.

Alessandro Isidori¹, Lorenza Borin², Elena Elli²

¹Hematology and Stem Cell Transplant Center, Marche Nord Hospital, Pesaro, Italy.

|April 28, 2018

Summary

Excess iron harms bone marrow by increasing oxidative stress and disrupting blood cell formation. Iron chelation therapy, like deferasirox, may protect against this toxicity and improve blood cell production.

Keywords:

Aplastic anemia Bone marrow microenvironment Hematopoietic stem cell transplantation Iron chelation Iron toxicity Myelodysplastic syndrome Myelofibrosis

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Area of Science:

Hematology
Toxicology
Molecular Biology

Background:

Excess iron is toxic, potentially causing organ damage without chelation therapy.
Iron toxicity impacts bone marrow by increasing reactive oxygen species and disrupting hematopoiesis.
Deferasirox, an iron chelator, shows potential in mitigating iron toxicity effects on the hematopoietic system.

Purpose of the Study:

To review the mechanisms of free iron toxicity in the bone marrow.
To explore the impact of iron toxicity on the hematopoietic microenvironment.
To discuss the potential role of deferasirox in counteracting iron-induced bone marrow damage.

Main Methods:

Literature review of preclinical studies on iron toxicity and bone marrow function.
Analysis of studies investigating deferasirox's effects on hematopoiesis.
Synthesis of current knowledge on iron metabolism and its impact on the hematopoietic microenvironment.

Main Results:

Iron toxicity generates reactive oxygen species, affecting gene expression related to hematopoiesis.
Iron chelation with deferasirox can partially reverse these detrimental effects.
Deferasirox may induce hematological responses and reduce transfusion dependency, though mechanisms are unclear.

Conclusions:

Free iron poses a significant risk to bone marrow function and the hematopoietic microenvironment.
Iron chelation therapy, particularly with deferasirox, offers a potential therapeutic strategy.
Further research is needed to elucidate the precise mechanisms by which deferasirox influences hematopoiesis in iron-overloaded states.