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Twenty-nine women and fifteen men from an area of low Se intake (South Island of New Zealand) consumed 100 micrograms stable 74Se, as selenate given in water after an overnight fast, and blood was collected for 3 weeks. They were then divided into five groups and supplemented with 0, 10, 20, 30 and 40 micrograms Se/d (as selenomethionine) for 5 months. After 5 months, they received a second dose of 74Se identical to the first. Supplementation significantly altered retention of 74Se in the plasma, but not in the erythrocytes or platelets. Subjects receiving the placebo retained the greatest amount, and subjects receiving 30 micrograms supplemental Se/d retained the least 74Se. Supplementation resulted in relatively more isotope being retained in a medium molecular mass protein considered to be albumin, and relatively less in another fraction considered to be selenoprotein P. The lack of many observed changes in retention of stable Se, and the shift in retention among the plasma proteins, suggests that supplemental Se was not being used to replete critical pools of Se, probably because of adaptation to low Se intake.

Thirty-six New Zealand women aged between 18 and 23 years received daily for 32 weeks, 200 micrograms Se as Se-enriched yeast (selenomethionine, SeMet), or brewer's yeast mixed with selenate, or no added Se (placebo) in a double-blind trial. Mean daily Se excretion increased with both supplements; the selenate group excreted more than the SeMet group, 123 v. 66 micrograms/d respectively at week 2, equivalent to 57 v. 27% of the dose. Thereafter Se output increased for the SeMet group reaching a plateau at about 100 micrograms/d at week 16, when plasma Se had also plateaued at 190 ng/ml. The selenate group had reached an earlier plateau of 110 ng Se/ml at week 7. There was a close relationship between 24 h urine and plasma Se for the SeMet group but not for the selenate group. Renal plasma clearances showed two distinctly different responses; the clearance of 0.4 ml/min reached by the SeMet group at week 2 plateaued as plasma Se increased almost 2-fold; whereas for the selenate group the clearance varied between 0.8 and 1.1 ml/min whilst plasma Se remained almost constant at 110 ng/ml. Previous studies, also of 200 micrograms Se/d as Se-rich bread, in New Zealand (NZ) and elsewhere showed similar responses to Se-yeast; the selenite response was intermediate between selenate and Se-yeast (SeMet). The full significance of these studies awaits identification of Se components in plasma, glomerular filtrate and urine; meanwhile renal clearances serve as a pointer to changes in the distribution of Se-containing fractions in the plasma. Trimethylselenonium was detected in basal urines, and was a minor component in urines of supplemented NZ subjects at about 1% of the total Se.

Thirty-three New Zealand women aged 18-23 years received daily for 32 weeks, 200 micrograms Se as Se-enriched yeast (selenomethionine), or brewer's yeast mixed with selenate, or no added Se (placebo) in a double-blind trial. Se supplementation raised (P = 0.001) platelet glutathione peroxidase (EC 1.11.1.9; GSHPx) activity, and also Se and GSHPx in whole blood, erythrocytes and plasma. Selenomethionine was more effective in raising blood Se concentrations than selenate, but both were equally effective in raising GSHPx activities in whole blood, erythrocytes and plasma, indicating a similar bioavailability for the two forms. These observations and those of gel filtration studies of erythrocytes and plasma proteins reported elsewhere (Butler et al. 1991) are consistent with the incorporation of Se from selenomethionine into a general tissue protein pool while selenate is directly available for GSHPx synthesis, and explain the poorer correlation between Se and GSHPx in individuals with higher Se status. However, selenate raised platelet GSHPx activities to a greater extent than did selenomethionine suggesting some other effect of selenate on platelets which needs further investigation. A response of GSHPx activity in these New Zealand subjects indicates that their dietary Se intake is insufficient to meet recommended intakes based on the criterion of saturation of GSHPx activity, and could reflect a marginal Se status. The level of blood Se necessary for saturation of GSHPx of about 100 ng Se/ml whole blood confirms observations in earlier studies.

Sodium selenite and selenomethionine were investigated as possible causative factors for the induction of Degnala disease syndrome in twelve buffalo (Bubalus bubalis) calves divided into three groups of four. Group 1 was the control group and received no additional selenium. Sodium selenite and selenomethionine were given daily as intramuscular injections on a selenium-equivalent basis, with a weekly increment in the dose of 0.05 mg Se/kg live weight from 0.05 to 0.20 mg Se/kg live weight per day, in groups 2 and 3 respectively. Only one animal from group 3 manifested the lesions of Degnala disease. The blood Se concentration and erythrocyte glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity were both greater in groups 2 and 3 than in control group 1. The overall blood Se concentration was 0.22 (SE 0.01), 0.38 (SE 0.12) and 0.77 (SE 0.20) micrograms Se/ml in groups 1 to 3 respectively with corresponding GSH-Px activities of 63.84 (SE 7.38), 88.37 (SE 12.38) and 165.32 (SE 40.62) enzyme units/mg protein. Erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2) activity was not affected by treatment but reduced glutathione content was lower in groups 2 and 3. Liver adenosylmethionine, estimated at autopsy, was lowest (22.87 (SE 6.17) mumol/g) in group 3, and greatest (102.63 (SE 9.39) mumol/g) in group 1 (P less than 0.01). Organic Se sources seemed to accumulate in tissues more than inorganic sources, and might be the causative toxic factors of Degnala disease.

1. [75Se]selenite of [75Se]selenomethionine was injected in to the coelomic cavity of fish. After 2 d or 14 d the muscle portion of the fish was removed and homogenized. The long-term fate in rats of an oral dose of each labelled homogenate was compared with that of an oral dose of [75Ee]selenite or [75Se]selenomethionine mixed with unlabelled fish homogenate. 2. Urinary and faecal radioactivity were measured during the 1st week and whole-body radioactivity was determined for 10 weeks. Rats were killed at weekly intervals for 4 weeks for analysis of tissue distribution of 75Se. 3. Intestinal absorption of 75Se given as labelled fish homogenate was less complete than that of 75Se mixed with unlabelled homogenate, and the absorption of 75Se from the 14 d-labelled fish homogenate derived from [75Se]selenite was less complete than that of 75Se from the other labelled homogenates. 4. Urinary excretion of absorbed 75Se in the first 7 d was in the range 5--8% absorbed dose and was slightly greater in the rats given 75Se as selenite or derived from selenite than in those given 75Se as selenomethionine or derived from selenomethionine. Endogenous faecal excretion of absorbed Se was similar in all groups, as also were tissue distribution of retained 75Se and long-term whole-body turnover rate. 5. The results of these studies are compared with those of earlier studies of the metabolism in rats of [75Se]selenomethionine, [75Se]selenite, [75Se]selenocystine and 75Se incorporated in vivo into rabbit kidney. There were differences in the initial utilization of 75Se from these various sources but after the 1st week 75Se from all sources appeared to be metabolized similarly, suggesting that for rats dietary Se of all forms is ultimately incorporated into the same metabolic pool.