Abstract
A specific chemical method was employed to measure B, compounds in men, pregnant and nonpregnant women, and fetal blood and urine before and after loading with pyridoxol. The blood levels of pyridoxal phosphate, the coenzyme form of the vitamin, were significantly lower in pregnancy, while fetal cord blood levels were high, indicating the existence of a relative deficiency state in pregnant women. In the various subjects examined, no differences were found in the urinary excretion of pyridoxic acid, the main metabolite of the vitamin, which suggests that intestinal absorption of the vitamin was unimpaired during pregnancy. Phosphorylation of pyridoxol was rapid in all subjects as blood levels of pyridoxal phosphate reached a peak 2 hours after oral and 10 minutes after intravenous loading. Pyridoxal phosphate levels in fetal blood reached a peak several hours after maternal blood indicating that the phosphorylated forms of the vitamin crossed the placental barrier to the fetus. Pyridoxol metabolism was unaffected during pregnancy, suggesting that the major cause of a relative maternal deficiency was as a result of the large fetal uptake of the vitamin.
Published Version
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