EFFECTS OF PYRIDOXINE DEFICIENCY AND DIETARY CHOLESTEROL SUPPLEMENTATION IN THE CHICK ON PLASMA PROTEIN-BOUND IODINE, GLUTAMIC–OXALACETIC TRANSAMINASE ACTIVITY, AND 14C-ACETATE INCORPORATION INTO CHOLESTEROL

The influence of B6 avitaminosis and the feeding of cholesterol on protein-bound iodine (PBI) of plasma and plasma glutamic–oxalacetic transaminase (PGOT) levels of chicks was studied, and the findings related to relative rates of 14C-acetate incorporation into plasma and liver cholesterol of chicks 3, 5, 11, and 15 days old.High plasma cholesterol levels were noted in the 11-day-old vitamin B6-deficient chicks. Liver cholesterol levels of this group were not significantly altered. Dietary cholesterol added at a level of 1% significantly increased liver and plasma cholesterol levels of the cholesterol-fed control and vitamin B6-deficient chicks; it also inhibited 14C-acetate incorporation into plasma and liver cholesterol to a much greater extent than did simple B6 avitaminosis or exogenous cholesterol per se. PBI parameters for control and vitamin B6-deficient chicks resembled those of plasma and liver cholesterol specific activity curves during the experimental period. Decreased PBI levels were noted 8 days after the beginning of the experiment in the vitamin B6-deficient birds. Dietary cholesterol significantly decreased PBI levels of 11-day-old control birds but increased it markedly 4 days later. PBI levels of the 11-day-old cholesterol-fed birds deficient in vitamin B6 were not changed, but were significantly increased 4 days later. PGOT levels were highest in 3-day-old control birds, and decreased rapidly thereafter. PGOT levels of the vitamin B6-deficient chicks were significantly decreased 3 to 4 days after the beginning of the experiment. The supplementary dietary cholesterol increased PGOT levels of 15-day-old cholesterol-fed control birds, but decreased PGOT levels of cholesterol-fed chicks deficient in vitamin B6. Although preliminary, these observations suggest an interrelationship between pyridoxine, thyroxine, and the mechanism responsible for the synthesis of cholesterol.