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105 , 121 , 126 Although the cause of hyperbilirubinemia in G6PD-deficient infants sometimes reflects accelerated red cell breakdown, 112 , 123 , 127 often there is no obvious RBC destruction or oxidant exposure
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Therapeutically, these cells can be further potentiated using agents that intensify iron release (e.g., NCOA4 activators), enhance ACSL4-mediated PUFA incorporation, or inhibit GPX4-stabilizing pathways (106)
The effect of Toxoplasma gondii and other parasites on activity levels in wild and hybrid Rattus norvegicus
