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doi: 10.1111/j.1742-1241.2009.02265.x 210 YangWChenLJiQLiuXMaJTandonNet al
Redox regulation of neutral sphingomyelinase-1 activity in HEK293 cells through a GSH-dependent mechanism
In Selenium 2011 (pp
This approach is part of our individualized treatment plans, supported by our medical team
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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