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Although mitochondrial respiration was noted as unchanged in resting and stimulated CD4+ and CD8+ T cells, CD8+ T cells were found to have a reduction in proton leak, ATP synthesis, and mitochondrial membrane potential (254)
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The possibility that sustained folic acid intake would deplete vitamin B-12 independent of hematopoiesis suggests a plausible alternative mechanism based on the known details of the renal handling of holoTC, whereby folic acid might interfere with holoTC reuptake or cause its sequestration in the kidney, promoting the excretion of holoTC and further depleting metabolically active vitamin B-12 during vitamin B-12 deficiency
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