[en] [³H]5'-O-(beta-D-glucopyranosyl) pyridoxine (PN-glucoside) and [¹⁴C]pyridoxine (PN) were orally administered to lactating rats. Milk was collected from the dam, and the stomach contents and liver were collected from the suckling pups 24 and 48 h after administration. Analysis of the isotopic ratio (³H/¹⁴C) in the milk and stomach contents indicated that the secretion of ³H in the milk was 20-25% as great as the secretion of ¹⁴C. The only labeled form of ³H and ¹⁴C in the stomach contents was pyridoxal phosphate (PLP), indicating that PN-glucoside was hydrolyzed to PN and subsequently metabolized prior to secretion by the mammary gland. The isotopic ratio in the livers of the pups was similar to that of the stomach contents. Furthermore, the relative distribution of the two isotopes among the hepatic metabolites of the pups was similar. The results of this study indicate that intact PN-glucoside is not secreted in milk, although vitamin B-6 derived from the limited hydrolysis and metabolism of PN-glucoside is delivered to the mammary gland for secretion

[en] [3H]5'-O-(beta-D-glucopyranosyl) pyridoxine (PN-glucoside) and [14C]pyridoxine (PN) were administered orally or intraperitoneally to vitamin B-6-adequate or -deficient rats. Analysis of intestinal contents and feces indicated effective intestinal absorption of PN-glucoside relative to PN. There was greater retention of 14C than 3H in the liver and carcass regardless of the route of administration of the radiolabeled vitamins. There was no major difference in the relative distribution of 3H and 14C among the vitamin B-6 metabolites in the liver between the treatment groups, and no [3H]PN-glucoside was detected in any of the livers. For all groups, the majority of the 3H administered was detected in the urine within 24 h. Less excretion of both 3H and 14C in the urine was observed for the deficient rats. There was no major difference in the relative proportion of urinary [3H]PN-glucoside or [3H]4-PA between rats fed or injected with the radiolabeled vitamins. These results indicate that vitamin B-6 status influences the clearance of metabolites derived from PN and PN-glucoside, as well as the clearance of intact PN-glucoside. Vitamin B-6 status, however, has little or no effect on the utilization of PN-glucoside. This study also suggests that the intestine is the primary site of the limited conversion of PN-glucoside to biologically active PN in the rat

[en] Mice given propylthiouracil, a thyroid inhibitor, and fed a diet containing a nontoxic level of rac-1(3)-palmitoyl glycerol showed the hypothermia and mortality expected for a toxic dose, but did not show these signs when linoleate or oleate was added to the diet. Loss of radioiodine from the whole animal and thyroid gland was slower when mice were fed the toxic palmitoyl glycerol diet than when fed the same diet containing 4% safflower oil. However, mice fed the two diets did not differ in the extent of the incorporation of radioiodine, and essentially all was bound to protein in each case. Follicular thyroid cells from mice fed the potentially toxic diet that contained unsaturated fat were normal in appearance. Conversely, cells from mice fed the toxic diet were smaller and more densely stained, showing evidence of glycoprotein inside the cell. These findings show that the thyroid gland is affected by the palmitoyl glycerol diet. However, the thyroid is not the only organ affected, because giving either thyroxine or triiodothyronine had no effect on the toxicity of palmitoyl glycerol