Dose-response relations in urinary excretion of trimethylselenonium in the rat.

75Se-labeled selenite was administered to fasting rats by orogastric intubation (1.5-3000 micrograms/kg body wt). Urine was collected and characterized for total radioactivity as well as for radiolabeled trimethylselenonium (TMSe). At lower doses of selenite (up to 500 micrograms/kg body wt), 30% of the administered dose was excreted. At higher doses of selenite, fractional urine excretion decreased as a function of the dose. The observed decrease in fractional urine excretion was not caused by changes in the absorption of the administered radiolabel. There was a direct relationship between the amount of the administered dose of selenite (up to 1500 micrograms/kg body wt) and the proportion of urinary [75Se] excreted as TMSe. Pretreatment with seleno compounds (10 or 100 micrograms Se/kg body wt as selenite, or selenomethionine) for 35 d before a challenge dose of [75Se]selenite did not influence the excretion of total [75Se] or of [75Se]TMSe in urine. Ingestion of a choline-deficient diet, which should deplete the availability of methyl groups, did not have any effect on excretion of total [75Se] or of [75Se]TMSe in urine after a challenge dose of [75Se]selenite (500 micrograms/kg body wt). The data presented here permit the following conclusions: 1) Production of TMSe is dose dependent, 2) production of TMSe from a single acute dose does not depend on the history of selenium intake and 3) rats fed a methyl-deficient diet are able to eliminate Se via formation of TMSe.

[Xanthurenuria at different stages of liver lesion induced by protein and choline deficiency]. / Izuchenie ksanturenurii na razlichnykh stadiiakh povrezhdeniia pecheni, vyzbannogo defitsitom belka i kholina.

The parallelism between xanthurenuria and liver affections caused by protein and choline deficiency was studied. At the stages marking the development of lipohepatosis and fibrosis there occurred an intensive passage of xanthurenic acid. The intensity of xanthurenuria at the stage marking the appearance of hyperplastic nodes continued to gain strength. With progressive advance of pathological changes, which by the 9--12th months of the experiment reached the stage of a fully developed nodular cirrhosis xanthurenuria gradually stopped.

[Influence of riboflavin on xanthuria leveloping as a result of protein and choline deficiency]. / O vliianii riboflavina na ksqnturenuriiu, voznikaiushchuiu pri defitsite belka i kholina

In growing male-rats intensively excreting xanthuric acid under the effect of rations deficient in protein and choline the passage of riboflavin with urine was determined. A series of tests with deficient choline in conjunction with a well-marked protein shortage revealed an intensive passage of riboflavin. On the other hand, a series of tests with deficient choline against the background of a moderate protein shortage failed to show any difference in the passage of riboflavin by test and control anomals. A single administration of 200 gamma of riboflavin to rats helped bring down elevated concentrations of xanthuric acid in the urine.