Selenoprotein P in Patients on Home Parenteral Nutrition

Rannem, T.; Persson-Moschos, M.; Huang, Wuqing; Staun, Michael; Åkesson, Björn

doi:10.1177/0148607196020004287

Cited by 14 publications

(9 citation statements)

References 31 publications

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“…Selenium is generally accepted as an essential component of total parenteral nutrition since in its absence deficiency symptoms are observed (198,292), and it has been shown to have a positive effect on immune function in patients on home parenteral nutrition for short-bowel syndrome (285).…”

Section: Selenium In Critical Illnessmentioning

confidence: 99%

Selenium in Human Health and Disease

Fairweather‐Tait

Bao

Broadley

et al. 2011

Antioxidants & Redox Signaling

1,072

820

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This review covers current knowledge of selenium in the environment, dietary intakes, metabolism and status, functions in the body, thyroid hormone metabolism, antioxidant defense systems and oxidative metabolism, and the immune system. Selenium toxicity and links between deficiency and Keshan disease and Kashin-Beck disease are described. The relationships between selenium intake/status and various health outcomes, in particular gastrointestinal and prostate cancer, cardiovascular disease, diabetes, and male fertility, are reviewed, and recent developments in genetics of selenoproteins are outlined. The rationale behind current dietary reference intakes of selenium is explained, and examples of differences between countries and/or expert bodies are given. Throughout the review, gaps in knowledge and research requirements are identified. More research is needed to improve our understanding of selenium metabolism and requirements for optimal health. Functions of the majority of the selenoproteins await characterization, the mechanism of absorption has yet to be identified, measures of status need to be developed, and effects of genotype on metabolism require further investigation. The relationships between selenium intake/status and health, or risk of disease, are complex but require elucidation to inform clinical practice, to refine dietary recommendations, and to develop effective public health policies.

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Section: Selenium In Critical Illnessmentioning

confidence: 99%

Selenium in Human Health and Disease

Fairweather‐Tait

Bao

Broadley

et al. 2011

Antioxidants & Redox Signaling

1,072

820

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show abstract

“…Its concentration in plasma re¯ects the selenium status in healthy subjects (Marchaluk et al, 1995;Persson-Moschos et al, 1995a;Hill et al, 1996) as well as in patients with low selenium status (Persson-Moschos et al, 1995b;Rannem et al, 1996). Selenoprotein P is a selenium-rich protein, which contains up to ten selenocysteine residues per polypeptide chain, compared to one selenocysteine residue in other characterised selenoproteins.…”

Section: Introductionmentioning

confidence: 99%

Plasma selenoprotein P levels of healthy males in different selenium status after oral supplementation with different forms of selenium

1998

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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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“…A number of studies have shown that the concentration of selenium in body fluids in patients on parenteral nutrition depends on the amount of selenium supplied. Thirty-eight patients who had been on parenteral nutrition with no addition of selenium for 3 -216 months had a mean plasma concentration about half of that measured in healthy subjects [29]. Eighty-nine percent of the patients had SeP values lower than mean -2 SD of the reference material, and the lowest value observed was only 3% of the reference value.…”

Section: Sep During Depletion Of Selenium Statusmentioning

confidence: 89%

“…Later, preliminary data from a radioimmunoassay using polyclonal antibodies against human SeP was reported [10]. This assay was then further optimized [26] and employed in different studies [27][28][29][30][31][32][33]. The lowest level of SeP possible to detect thus far was 0.05 arbitrary units, which corresponds to approximately 3% of the normal mean value for plasma SeP.…”

Section: Analysis Of Sepmentioning

confidence: 99%

“…For subjects in different European regions, the correlation between SeP and plasma selenium was generally more marked in areas with low plasma selenium [27]. In patients with malabsorption due to intestinal disease with a mean plasma selenium concentration of only 0.5 mmol/l, the SeP level was likewise highly correlated with plasma selenium (r =0.91) [29]. The lower correlations at higher plasma selenium concentrations may largely be due to the SeP level approaching a plateau at selenium concentrations in the range of 1.2-1.5 mmol/l.…”

Section: The Relation Of Sep To Other Biomarkers Of Selenium Status Imentioning

confidence: 99%

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Selenoprotein P

Moschos¹

2000

CMLS, Cell. Mol. Life Sci.

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Selenoprotein P (SeP) is an extracellular, monomeric glycoprotein containing up to 10 selenocysteine residues in the polypeptide chain. It is ubiquitously expressed in mammalian tissues, and in human plasma it accounts for at least 40% of the total selenium concentration. SeP binds to heparin and cell membranes, and is associated with endothelial cells. SeP in human plasma protects against peroxynitrite-mediated oxidation and reduces phospholipid hydroperoxide in vitro, in accordance with the presumption that it has a function as an extracellular oxidant defense. Immunochemical assays have demonstrated that its concentration in plasma varies much with selenium intake, but other factors also have an influence.

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Selenoprotein P in Patients on Home Parenteral Nutrition

Abstract: The positive correlations between selenoprotein P and eGSHPX and plasma selenium indicates that selenoprotein P may be used as a marker of selenium status in selenium-depleted patients.

Cited by 14 publications

References 31 publications

Selenium in Human Health and Disease

Selenium in Human Health and Disease

Plasma selenoprotein P levels of healthy males in different selenium status after oral supplementation with different forms of selenium

Selenoprotein P

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