Groups of 7-12 weanling Sprague-Dawley male rats were fed graded daily doses of vitamin A (5-176 micrograms retinol) for 7 or 12 weeks. Final mean liver concentrations of vitamin A, which ranged from 0.4 to 331 micrograms retinol per gram, depended both on the daily dose given and on the length of the feeding period. The mean serum retinol concentration was 24 micrograms/dl at the lowest liver vitamin A concentration, approached a plateau of 40 micrograms/dl at a liver concentration of 5-10 micrograms/g, and then very slowly increased with higher levels of vitamin A in the liver. Seven days after the oral administration of a standard dose (4.6 microCi) of 11,12-[3H2]retinyl acetate, during which period rats were fed the customary vitamin A-containing diet, bile was collected via bile duct cannulae for 1-4 hours, and then the livers and serum were extracted and analyzed. The key relationships defined were: 1) that the mean ratio of specific activities of retinol in serum to that in liver was 0.65 +/- 0.05 (SEM) (range: 0.46-0.81) at daily retinol intakes of 8-176 micrograms/day, 2) that the ratio did not vary systematically with vitamin A intake or liver reserves and 3) that the mean excretion rate of vitamin A metabolites in the bile was invariant at 0.28 microgram retinol metabolites per milliliter of bile up to a liver vitamin A concentration of 32 micrograms retinol per gram, but then increased rapidly by eightfold to a maximal rate of 2.4 micrograms retinol metabolites per milliliter of bile at a liver vitamin A value of 140 micrograms retinol per gram.(ABSTRACT TRUNCATED AT 250 WORDS)

To assess the age-dependent vitamin A status of children, liver samples taken at autopsy from 170 American children 0-15 yr of age were analyzed for vitamin A and carotenoids. The median liver vitamin A concentration at birth was low (11 micrograms retinol/g), remained constant to 3 mo, rapidly increased to 4 yr (130 micrograms/g) and then remained constant into adolescence. In contrast the vitamin A status of premature infants deteriorated after birth. Of infants less than 3 mo, approximately one-fourth and two-thirds showed liver vitamin A concentrations less than or equal to 5 micrograms retinol/g and less than or equal to 20 micrograms/g, respectively. On the other hand, essentially all infants greater than or equal to 6 months showed an adequate vitamin A status, defined as liver stores greater than 20 micrograms retinol/g liver. Liver carotenoid concentrations did not meaningfully correlate with age or with vitamin A concentrations. Parameters that did not significantly affect the vitamin A concentration were: 1) height and weight in infants less than 1 mo, except in the highest weight-height groups, 2) sex, although values of females were slightly higher than males, and 3) causes of death.

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When single large equimolar doses (0.38-0.41 mmol/kg BW) of all-trans retinoic acid (RA), all-trans retinoyl beta-glucose (RBGL), and all-trans retinoyl beta-glucuronide (RBG) are administered orally in oil on day 8.5 of pregnancy to Sprague-Dawley rats, RA and RBGL proved highly teratogenic, whereas RBG was not. Indeed, fetuses from RBG-treated dams were 16% heavier (P < 0.01) than control fetuses. After dosing with RA and RBGL, RA appeared in large amounts within 0.5 h in the maternal plasma and within 1.0 h in the embryo. In contrast, orally administered RBG seemed to be absorbed much more slowly, to be converted very slowly to RA, and not to accumulate either as RBG or as RA in the embryo. When incubated in vitro with embryos and attached membranes, however, both all-trans RBG and all-trans RA were partially converted to 13-cis RA. The nonteratogenicity of RBG, in contrast to RA, seems to be due to a much slower rate of GI absorption, a slow rate of hydrolysis to RA, a limited passage from the maternal circulation into the embryo, and a lower inherent toxicity.

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