Some characteristics of a radioimmunoassay of selenoprotein P (a major selenoprotein in human serum) are described. Polyclonal antibodies generated in rabbits were used and goat anti-rabbit-IgG antiserum was used as a second antibody. Depending on the concentration of selenoprotein P, 1-10 microliters of human serum were used in the assay. The relative standard deviation for the concentration of selenoprotein P was 6.3% between assays and 7.7% within assays. Different animal sera gave no significant interference, indicating that the antibodies did not react with non-human analogues of selenoprotein P. No indication of cross-reactivity could be found concerning extracellular glutathione peroxidase (another selenoprotein in serum). Addition of increasing amounts of normal human serum and partially purified selenoprotein P to the radioimmunoassay resulted in parallel curves. Incubation at 4 degrees C gave somewhat higher binding of labelled selenoprotein P than incubation at room temperature. The epitope, recognized by the antibodies, was apparently stable after storage of serum (in the frozen state for years, and in the cold for months). No significant amount of selenoprotein P could be demonstrated in red blood cells, and analysis of haemolysed whole blood gave expected data. Investigations of selenium status in different study groups indicated that in most cases the concentration of selenoprotein P in serum was positively correlated to that of glutathione peroxidase and serum selenium. In an intervention study, where subjects decreased their selenium intake to 50%, the serum levels of glutathione peroxidase and selenium decreased, but no significant decrease of selenoprotein P could be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Objective: To assess changes in selenoprotein P levels in plasma from subjects who had received oral supplements of different selenium forms. Design: The same study group participated in two similar selenium supplementation trials, Trial I in 1981(Levander et al, 1983 and Trial II in 1987(Alfthan et al, 1991. During Trial II the mean baseline intake of selenium in Finland was higher compared to that during Trial I (100 and 40 mg/d, respectively), due to a nationwide supplementation of fertilisers which started in 1985. Subjects: Fifty healthy Finnish men, 36±60 y old. Intervention: The study group received daily placebo or oral supplements consisting of 200 mg selenium as selenium-enriched yeast, sodium selenate or selenium-enriched wheat (Trial I) or selenium-enriched yeast, sodium selenate or sodium selenite (Trial II). The duration of supplementation periods was 11 (Trial I) and 16 (Trial II) weeks. Results: In Trial I the mean plasma selenoprotein P values in all the supplemented groups increased signi®cantly, approaching a plateau at 2 weeks and reaching maxima at 4 weeks (mean increase 34%, P`0.05). In Trial II the mean selenoprotein P levels of the supplemented groups were not signi®cantly different from each other or from the placebo group at the start or at any time point of the supplementation period. Conclusions: At a low selenium status the selenoprotein P levels increased in a similar fashion after supplementation with different forms of selenium, but at a high selenium status no signi®cant effects of supplementation with the same amount of selenium were observed. No differences in selenoprotein P levels were observed for inorganic and organic selenium supplements.

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Objective: To study the relationships between ®sh intake and different markers of selenium status and thyroid hormone function. Design: Cross-sectional study. Setting and subjects: Sixty-eight men (age 24±79 years) were recruited among coastal ®shermen and inland subjects from Latvia. None of the subjects was on selenium medication or had any known endocrine disease. Main outcome measures: Correlations between ®sh intake, plasma levels of selenium, selenoprotein P, glutathione peroxidase, organic mercury in erythrocytes and TSH in serum. Results: Selenium in plasma ranged from 0.30 to 1.56 mmola1, selenoprotein P from 0.54 to 2.21 arbitrary units relative to pooled plasma, and glutathione peroxidase from 1.20 to 5.73 mga1. The number of ®sh meals per month was correlated with plasma selenium, selenoprotein P and glutathione peroxidase (r 0.63, r 0.62 and r 0.50, respectively; P`0.001). Plasma selenium was correlated with selenoprotein P and glutathione peroxidase (r 0.88 and r 0.67, respectively; P`0.001), and also selenoprotein P and glutathione peroxidase were correlated (r 0.63, P`0.001). The mean plasma selenium level in those with a high ®sh intake (21±50 ®sh mealsamonth), was 81% higher than in those with lowest ®sh intake. TSH in serum was inversely correlated with plasma selenium and selenoprotein P. Thyroid hormone levels were not correlated with plasma selenium, selenoproteins or ®sh intake. Conclusions: In this study group, selenium from ®sh intake had a marked impact on all variables studied on selenium status. No impact of selenium status on T3 and T4 levels was observed. The slightly negative correlation of selenium status with TSH levels might indicate a higher TSH secretion at low selenium status.

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