By A.L & Schwartz, Morton Latner
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Additional resources for Advances in Clinical Chemistry, Vol. 23
The plasma pyridoxal levels in the affected group returned to normal after treatment with 100mg of oral pyridoxine for 7 days, and there was significant clinical improvement. Depressive illnesses in oral contraceptive users have been related to relative pyridoxal phosphate deficiency; therefore it is not surprising that postpartum depression should be considered from this point of view, assum- CLINICAL CHEMISTRY OF VITAMIN B6 33 ing that in some women the state of vitamin B, deficiency produced during pregnancy, coupled with a possible derangement of brain 5-hydroxytryptophan decarboxylase (a pyridoxal phosphate-dependent enzyme), leads to decreased brain 5-hydroxytryptamine and, hence, depression.
Complexes of pyridoxal phosphate bound to dietary protein, such as Epyridoxyllysine, have in rats only 60% of the molar potency of pyridoxine CLINICAL CHEMISTRY OF VITAMIN Be 23 (G10). Pyridoxal phosphate also forms cyclic compounds with histamine and histidine (K10) which may interfere with absorption of the vitamin. Antagonists. Drugs can impair vitamin absorption, increase vitamin excretion, or interfere with vitamin utilization. Such drug-induced deficiency can occur even when the diet is adequate for normal maintenance.
Feltkamp et al. (F3)could not show any significant difference in erythrocyte asparate aminotransferase index values for a small group of oral contraceptive users compared to controls, but did observe that when given 300 mg of pyridoxine hydrochloride daily for 3 months, there was an increase in basal erythrocyte asparate aminotransferase activity, but that the saturation index fell to normal due to saturation of the enzyme with cofactor. The increased basal enzyme activity [on a dose 10 times that recommended by Luhby (L12)] was explained by induction of the red cell enzyme, indicating yet another factor which needs careful attention if vitamin status is to be adequately assessed.