ABSTRACT
Normal subjects received fenretinide (HPR), 200 mg/d, on three schedules. Schedule 1 was treatment for 28 d. Schedule 2 consisted of 14 d of treatment, 3 d hiatus, and a second drug course of 14 d, 10,000 IU vitamin A was administered during the 3-d hiatus. Schedule 3 was 14 d of treatment followed by a rest period of 7 d and then 14 d of treatment. Increase in plasma HPR was accompanied by an even higher increase in the metabolite N-(4-methoxyphenyl)-all-trans-retinamide (MPR). The administration of HPR was associated with a significant reduction in retinol-binding protein (RBP), which returned to pretreatment values after the drug treatment was discontinued. Reduction of plasma retinol was also observed. Use of interrupted schedules with resting periods of 3 and 7 d changed HPR, MPR, and RBP concentrations in plasma. Addition of vitamin A did not affect the pattern of the measured variables in the plasma.
Subject(s)
Retinol-Binding Proteins/metabolism , Tretinoin/analogs & derivatives , Adult , Drug Administration Schedule , Female , Fenretinide , Humans , Male , Retinol-Binding Proteins, Plasma , Tretinoin/metabolism , Tretinoin/pharmacokinetics , Tretinoin/pharmacology , Vitamin A/bloodABSTRACT
The effect of selenium on immune responses in animals and humans is controversial. It has been reported that phagocytosis as a part of the immune function is affected by selenium deficiency. We conducted a study to investigate the effect of selenium on the phagocytic function of polymorphonuclear leukocytes (PMNs) in normal healthy individuals before and after selenium supplementation. Ingestion of sodium selenite 400 micrograms/day (182.8 micrograms pure selenium) resulted in a significant increase in plasma selenium levels. The phagocytic function of PMNs was measured by ingestion of Oil Red O paraffin droplets and chemiluminescence tests. The phagocytic function was increased, but the results before and after selenium supplementation were not significant. It was concluded that inorganic selenium was not an efficient stimulating agent of phagocytosis in humans.