The suicidal death of erythrocytes should be considered a possible cause of hemolysis and
plasma bilirubin overload when there is no evidence of an immune-mediated hemolytic anemia, no
consumptive red blood cell disorder, no morphologic or laboratory data to suggest a problem of the
red cell membrane, and no evidence of a quantitative or qualitative defect in hemoglobin synthesis.
In neonatal period, xenobiotics, cytokines, osmotic shock, energy depletion, oxidative stress, and
variation of temperature may induce an alteration of balance between damaging and protecting factors
which can be followed by red cell death. The intraerythrocyte redox balance plays a pivotal role
in orchestrating the complex molecular mechanisms leading to eryptosis.
Neonatal erythrocytes are a target of extracellular free radicals and, at the same time, are themselves
generators of free radicals through the Fenton reaction.
This review clarifies the complex mechanisms underlying the susceptibility of neonatal erythrocytes
to increased oxidative stress.