Selenoprotein P

Moschos, M. Persson

doi:10.1007/pl00000665

Cited by 61 publications

(14 citation statements)

References 52 publications

(91 reference statements)

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“…Apart from the systemic inflammatory response, selenium deficiency should be understood as a true low selenium status with decreased tissue selenoenzyme activity [39] and that this deficiency leads to low plasma selenium concentration, as well as low selenoprotein P or glutathione peroxidase [40,41]. In addition, considering that selenium content in plasma is a very small part of body selenium content (0.5 to 1%) one cannot deduce from a low plasma selenium concentration a low tissue selenoenzyme activity and thus a true selenium deficiency [3].…”

Section: Discussionmentioning

confidence: 99%

Low plasma selenium concentrations in critically ill children: the interaction effect between inflammation and selenium deficiency

et al. 2014

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IntroductionLow plasma selenium concentrations are frequent in critically ill patients. However, whether this is due to systemic inflammation, a deficient nutritional state or both is still not clear. We aimed to determine the factors associated with low plasma selenium in critically ill children while considering the inflammatory response and nutritional status.MethodA prospective study was conducted in 173 children (median age 34 months) with systemic inflammatory response who had plasma selenium concentrations assessed 48 hours after admission and on the 5th day of ICU stay. The normal reference range was 0.58 μmol/L to 1.6 μmol/L. The outcome variable was ‘low plasma selenium’, which was defined as plasma selenium values below the distribution median during this period. The main explanatory variables were age, malnutrition, sepsis, C-reactive protein (CRP), and clinical severity scores. The data were analyzed using a Binomial Generalized Estimating Equations model, which includes the correlation between admission and 5th day responses.ResultsMalnutrition and CRP were associated with low plasma selenium. The interaction effect between these two variables was significant. When CRP values were less than or equal to 40 mg/L, malnutrition was associated with low plasma selenium levels (odds ratio (OR) = 3.25, 95% confidence interval (CI) 1.39 to 7.63, P = 0.007; OR = 2.98, 95% CI 1.26 to 7.06, P = 0.013; OR = 2.49, 95% CI 1.01 to 6.17, P = 0.049, for CRP = 10, 20 and 40 mg/L, respectively). This effect decreased as CRP concentrations increased and there was loose significance when CRP values were >40 mg/L. Similarly, the effect of CRP on low plasma selenium was significant for well-nourished patients (OR = 1.13; 95% CI 1.06 to 1.22, P <0.001) but not for the malnourished (OR = 1.03; 95% CI 0.99 to 1.08, P = 0.16).ConclusionsThere is a significant interaction between the magnitude of the inflammatory response and malnutrition on low plasma selenium. This interaction should be considered when interpreting plasma concentrations as an index of selenium status in patients with systemic inflammation as well as in the decision on selenium supplementation.

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Section: Discussionmentioning

confidence: 99%

Low plasma selenium concentrations in critically ill children: the interaction effect between inflammation and selenium deficiency

et al. 2014

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“…Although P-Se reflects recent intake (Combs 2001), Se remains high throughout the year in this population, despite some seasonal variation (Lemire et al 2009). More than 40% of the Se in human plasma is bound to selenoprotein P (SelP) (Moschos 2000). Plasma SelP is the main transport form of Se for delivery and supporting essential physiological functions of Se in kidney, testis, and brain.…”

Section: Discussionmentioning

confidence: 99%

Selenium and Mercury in the Brazilian Amazon: Opposing Influences on Age-Related Cataracts

Lemire

Fillion

Frenette

et al. 2010

Environ Health Perspect

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BackgroundAge-related cataracts (ARCs) are an important cause of blindness in developing countries. Although antioxidants may be part of the body’s defense to prevent ARC, environmental contaminants may contribute to cataractogenesis. In fish-eating populations of the lower Tapajós region, elevated exposure to mercury (Hg) has been reported, and blood levels of selenium (Se) range from normal to very high (> 1,000 μg/L).ObjectivesWe examined ARCs in relation to these elements among adults (≥ 40 years of age) from 12 riverside communities.MethodsParticipants (n = 211) provided blood samples and underwent an extensive ocular examination. Inductively coupled plasma mass spectrometry was used to assess Hg and Se in blood and plasma.ResultsOne-third (n = 69; 32.7%) of the participants had ARC. Lower plasma Se (P-Se; < 25th percentile, 110 μg/L) and higher blood Hg (B-Hg; ≥ 25th percentile, 25 μg/L) were associated with a higher prevalence odds ratio (POR) of ARC [adjusted POR (95% confidence interval), 2.69 (1.11–6.56) and 4.45 (1.43–13.83), respectively]. Among participants with high P-Se, we observed a positive but nonsignificant association with high B-Hg exposure, whereas among those with low B-Hg, we observed no association for P-Se. However, compared with the optimum situation (high P-Se, low B-Hg), the POR for those with low P-Se and high B-Hg was 16.4 (3.0–87.9). This finding suggests a synergistic effect.ConclusionOur results suggest that persons in this population with elevated Hg, the cataractogenic effects of Hg may be offset by Se. Because of the relatively small sample size and possible confounding by other dietary nutrients, additional studies with sufficient power to assess multiple nutrient and toxic interactions are required to confirm these findings.

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“…Selenoprotein P is the most important selenium binding protein, which accounts for at least 40% of total plasma selenium load [67]. The protein contains a polymorphism in codon 234, the alanine allele being associated with lower plasma selenium concentrations in men, which affect GPx activity [68].…”

Section: Other Nuclear-encoded Mitochondrial Proteins Discussed In Camentioning

confidence: 99%

Mitochondrial and Nuclear Genes of Mitochondrial Components in Cancer

Kirches

2009

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Although the observation of aerobic glycolysis of tumor cells by Otto v. Warburg had demonstrated abnormalities of mitochondrial energy metabolism in cancer decades ago, there was no clear evidence for a functional role of mutant mitochondrial proteins in cancer development until the early years of the 21st century. In the year 2000, a major breakthrough was achieved by the observation, that several genes coding for subunits of the respiratory chain (ETC) complex II, succinate dehydrogenase (SDH) are tumor suppressor genes in heritable paragangliomas, fulfilling Knudson’s classical two-hit hypothesis. A functional inactivation of both alleles by germline mutations and chromosomal losses in the tumor tissue was found in the patients. Later, SDH mutations were also identified in sporadic paragangliomas and pheochromocytomas. Genes of the mitochondrial ATP-synthase and of mitochondrial iron homeostasis have been implicated in cancer development at the level of cell culture and mouse experiments. In contrast to the well established role of some nuclear SDH genes, a functional impact of the mitochondrial genome itself (mtDNA) in cancer development remains unclear. Nevertheless, the extremely high frequency of mtDNA mutations in solid tumors raises the question, whether this small circular genome might be applicable to early cancer detection. This is a meaningful approach, especially in cancers, which tend to spread tumor cells early into bodily fluids or faeces, which can be screened by non-invasive methods.

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Selenoprotein P

Cited by 61 publications

References 52 publications

Low plasma selenium concentrations in critically ill children: the interaction effect between inflammation and selenium deficiency

Low plasma selenium concentrations in critically ill children: the interaction effect between inflammation and selenium deficiency

Selenium and Mercury in the Brazilian Amazon: Opposing Influences on Age-Related Cataracts

Mitochondrial and Nuclear Genes of Mitochondrial Components in Cancer

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