Dataset Information

Selenium supplementation improves antioxidant capacity in vitro and in vivo in patients with coronary artery disease The SElenium Therapy in Coronary Artery disease Patients (SETCAP) Study.

ABSTRACT:

Background

Selenium is a central determinant of antioxidative glutathione peroxidase 1 (GPx-1) expression and activity. The relevance of selenium supplementation on GPx-1 in coronary artery disease (CAD) needs to be established. We assessed the effect of selenium supplementation on GPx-1 in cell culture and on endothelial function in a prospective clinical trial.

Methods

Human coronary artery endothelial cells were incubated with 5.78 to 578 nmol/L sodium selenite, Se-methyl-selenocysteine hydrochloride, or seleno-l-methionine. Glutathione peroxidase 1 mRNA and protein expression and activity were measured. Coronary artery disease patients (n = 465) with impaired endothelial function (flow-mediated dilation [FMD] <8%) were randomly assigned to receive 200 or 500 microg sodium selenite daily or matching placebo during a 12-week period. We tested the effect on red blood cell GPx-1 activity and brachial artery FMD. Furthermore, differences in biomarkers of oxidative stress and inflammation were measured.

Results

Sodium selenite and Se-methyl-selenocysteine hydrochloride increased GPx-1 protein and activity in a dose-dependent manner (P < .0001). The intention-to-treat groups comprised 433 CAD patients. Glutathione peroxidase 1 activity increased from 37.0 U/gHb (31.3-41.7) to 41.1 U/gHb (35.2-48.4) (P < .0001) in the 200 microg and from 38.1 U/gHb (33.2-43.8) to 42.6 U/gHb (35.0-49.1) (P < .0001) in the 500 microg sodium selenite group treated for 12-weeks. No relevant changes were observed for FMD or biomarkers of oxidative stress and inflammation.

Conclusions

Sodium selenite supplementation increases GPx-1 activity in endothelial cells and in CAD patients. Future studies have to demonstrate whether long-term CAD outcome can be improved.

SUBMITTER: Schnabel R

PROVIDER: S-EPMC3624729 | biostudies-literature | 2008 Dec

REPOSITORIES: biostudies-literature

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Publications

Selenium supplementation improves antioxidant capacity in vitro and in vivo in patients with coronary artery disease The SElenium Therapy in Coronary Artery disease Patients (SETCAP) Study.

Schnabel Renate R Lubos Edith E Messow Claudia M CM Sinning Christoph R CR Zeller Tanja T Wild Philipp S PS Peetz Dirk D Handy Diane E DE Munzel Thomas T Loscalzo Joseph J Lackner Karl J KJ Blankenberg Stefan S

American heart journal 20081201 6

<h4>Background</h4>Selenium is a central determinant of antioxidative glutathione peroxidase 1 (GPx-1) expression and activity. The relevance of selenium supplementation on GPx-1 in coronary artery disease (CAD) needs to be established. We assessed the effect of selenium supplementation on GPx-1 in cell culture and on endothelial function in a prospective clinical trial.<h4>Methods</h4>Human coronary artery endothelial cells were incubated with 5.78 to 578 nmol/L sodium selenite, Se-methyl-selen ...[more]

PMID: 19033020

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Project description:The disruption of endothelial homeostasis is the hallmark of coronary artery disease (CAD) and psychological disorders such as anxiety/depression. Xinkeshu (XKS), a traditional Chinese patent medicine, plays an essential role in CAD and psychological condition; however, the mechanisms underlying the effects of XKS on the endothelial function and endogenous endothelium-repair capacity in CAD patients with anxiety/depression remain elusive. In this study, endothelial function and endothelial progenitor cell- (EPC-) mediated reendothelialization capacity were compared among age-matched healthy subjects, CAD patients with or without anxiety/depression. Besides, CAD patients with anxiety/depression received 1-month XKS treatment. Anxiety/depression symptoms were evaluated by Generalized Anxiety Disorder 7-item (GAD-7)/Patient Health Questionnaire-9 (PHQ-9) score, endothelial function was tested by flow mediated dilation (FMD) measurement, and EPC-mediated reendothelialization capacity was evaluated by a carotid artery injury model in nude mouse (n = 6) with the injection of XKS-incubated EPCs from CAD patients with anxiety/depression. The results showed that FMD and EPC-mediated reendothelialization capacity of CAD patients with anxiety/depression were compromised compared to healthy subjects and CAD patients without anxiety/depression. After 1 month of XKS treatment, FMD increased from 4.29 ± 1.65 to 4.87 ± 1.58% (P < 0.05) in CAD patients with anxiety/depression, whereas it remained unchanged in the controls. Moreover, XKS decreased GAD-7 and PHQ-9 scores. Meanwhile, incubating XKS enhanced in vivo reendothelialization capacity and in vitro apoptosis of EPCs from CAD patients with anxiety/depression, which was associated with the upregulation of CXC-chemokine receptor 7 (CXCR7) and inhibition of phosphorylation of p38 signaling. CXCR7 knockdown abolished the beneficial effects of XKS, which was rescued by p38 inhibitor SB203580. Our data demonstrate for the first time that XKS improves endothelial function and enhances EPC-mediated reendothelialization through CXCR7/p38/cleaved casepase-3 signaling and provides novel insight into the detailed mechanism of XKS in maintaining endothelial homeostasis in CAD patients with anxiety/depression.

Project description:This study evaluated the effects of selenium (Se) supplementation in maternal and offspring diets on performance and antioxidant capacity of ducklings aged from 0 to 2 wk. A total of 144 female Longyan duck breeders aged 22-wk were allotted into 2 treatments and fed a control diet or a 0.16 mg Se/kg supplemented diet. At 40-wk, 120 offspring from each treatment were divided into 2 groups, with 6 replicates of 10 birds. Using a 2 × 2 factorial design, ducklings from each maternal dietary treatment were assigned to a control diet or a 0.16 mg Se/kg supplemented diet from hatch to 2-wk. Compared with Se-deficient diet, maternal diet supplemented with 0.16 mg Se/kg increased the BW of hatchlings (P < 0.01). There were interactions between maternal and progeny diet with 0.16 mg Se/kg in BW of ducklings aged 2 wk and BW gain (BWG) as ducklings from maternal Se/progeny none treatment had the lightest BW and BWG (P < 0.01). Maternal diet with 0.16 mg Se/kg decreased plasma concentration of uric acid and insulin-like growth factor 1 (P < 0.01), and progeny diet supplemented with 0.16 mg Se/kg increased the activities of glutathione peroxidase 3 (GPx3) in plasma and glutathione peroxidase 1 in erythrocyte (P < 0.01). Maternal diet with 0.16 mg Se/kg increased (P < 0.05) the hepatic activity of total superoxide dismutase (T-SOD). Progeny diet supplemented with 0.16 mg Se/kg increased (P < 0.01) hepatic activity of GPx3 and decreased (P < 0.01) the hepatic concentration of malondialdehyde. Interactions were detected between maternal and progeny diet with 0.16 mg Se/kg in hepatic activity of T-SOD and maternal and progeny diet supplemented with Se displayed the highest hepatic activity of T-SOD (P < 0.05). Overall, Se supplementation in the diet of duck breeders and offspring increased the antioxidant capacity of ducklings. Maternal Se supplementation increased the BW of hatchlings, whereas maternal and progeny dietary Se supplementation did not affect the BWG of ducklings aged from 0 to 2 wk. Se supplementation with additional 0.16 mg/kg in the diet of duck breeders and offspring displayed beneficial effects particularly on the antioxidant capacity in ducklings.

Dataset Information

Selenium supplementation improves antioxidant capacity in vitro and in vivo in patients with coronary artery disease The SElenium Therapy in Coronary Artery disease Patients (SETCAP) Study.

Background

Methods

Results

Conclusions

Publications

Selenium supplementation improves antioxidant capacity in vitro and in vivo in patients with coronary artery disease The SElenium Therapy in Coronary Artery disease Patients (SETCAP) Study.

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