Regulation of cellular glutathione peroxidase by different forms and concentrations of selenium in primary cultured bovine hepatocytes

Wu, Xianshi; Huang, Kehe; ChengWu, Wei; Fu, Chen; Chen, Pan

doi:10.1016/j.jnutbio.2008.12.006

Cited by 32 publications

(39 citation statements)

References 40 publications

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“…This result is consistent with Se affecting GPx protein through at least two mechanisms, mRNA stability, and level of Sec regulating translation [27]. We have previously observed a similar differential effect in bovine hepatocytes [28], when GPx1 mRNA was increased 3- to 6-fold, while GPx1 activity was 1.3- to1.5-fold higher.…”

Section: Discussionsupporting

confidence: 89%

Selenium Promotes T-Cell Response to TCR-Stimulation and ConA, but Not PHA in Primary Porcine Splenocytes

et al. 2012

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There is controversy in the literature over whether the selenium (Se) influences cellular immune responses, and the mechanisms possibly underlying these effects are unclear. In this study, the effects of Se on T-cell proliferation and IL-2 production were studied in primary porcine splenocytes. Splenocytes were treated with different mitogens in the presence of 0.5–4 µmol/L sodium selenite. Se significantly promoted T-cell receptor (TCR) or concanavalin A (ConA)-induced T-cell proliferation and IL-2 production but failed to regulate T-cell response to phytohemagglutinin (PHA). In addition, Se significantly increased the levels of cytosolic glutathione peroxidase (GPx1) and thioredoxin reductase 1 (TR1) mRNA, the activity of GPx1 and the concentration of reduced glutathione (GSH) in the unstimulated, or activated splenocytes. These results indicated that Se improved the redox status in all splenocytes, including unstimulated, TCR, ConA and PHA -stimulated, but only TCR and ConA-induced T-cell activation was affected by the redox status. N-acetylcysteine (NAC), a pharmacological antioxidant, increased T-cell proliferation and IL-2 production by TCR and ConA stimulated splenocytes but had no effect on the response to PHA in primary porcine splenocytes confirming that PHA-induced T-cell activation is insensitive to the redox status. We conclude that Se promotes GPx1 and TR1 expression and increases antioxidative capacity in porcine splenocytes, which enhances TCR or ConA -induced T-cell activation but not PHA-induced T-cell activation. The different susceptibilities to Se between the TCR, ConA and PHA -induced T-cell activation may help to explain the controversy in the literature over whether or not Se boosts immune responses.

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Section: Discussionsupporting

confidence: 89%

Selenium Promotes T-Cell Response to TCR-Stimulation and ConA, but Not PHA in Primary Porcine Splenocytes

et al. 2012

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“…41 According to the report of Wu et al, 42 the incubation of bovine hepatocytes for 24 hours with Se supplied as selenomethionine, Na 2 SeO 3 , or kappa selenocarrageenan at doses of 0.5-5.0 µmol/L, reduced intracellular GSH concentrations compared with controls. Previous research has also indicated that increasing the Na 2 SeO 3 concentration in the culture medium decreased the level of intracellular GSH in rabbit hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

Effect of selenium nanoparticles with different sizes in primary cultured intestinal epithelial cells of crucian carp, Carassius auratus gibelio

Li¹,

Yan²,

Fu³

2013

IJN

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“…However, it has been verified in some in vivo studies that the consumption of food supplemented with Se either as sodium selenite, Se-enriched yeast and/or selenomethionine increases mRNA levels of GPx (GPx-1, GPx-4) and TrxRs (TrxR-1) genes in different organs, e.g. liver, kidney, thyroid and testis [84,85,86]. In accordance, we observed that diphenyl diselenide intake per se enhanced the cerebral expression of GPx-1 and GPx-4 (cerebral cortex and striatum) and TrxR-1 and TrxR-2 (cerebral cortex).…”

Section: Discussionmentioning

confidence: 99%

Diphenyl Diselenide Modulates Gene Expression of Antioxidant Enzymes in the Cerebral Cortex, Hippocampus and Striatum of Female Hypothyroid Rats

Dias¹,

Golombieski

Portella³

et al. 2014

Neuroendocrinology

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Introduction: Cellular antioxidant signaling can be altered either by thyroid disturbances or by selenium status. Aims: To investigate whether or not dietary diphenyl diselenide can modify the expression of genes of antioxidant enzymes and endpoint markers of oxidative stress under hypothyroid conditions. Methods: Female rats were rendered hypothyroid by continuous exposure to methimazole (MTZ; 20 mg/100 ml in the drinking water) for 3 months. Concomitantly, MTZ-treated rats were either fed or not with a diet containing diphenyl diselenide (5 ppm). mRNA levels of antioxidant enzymes and antioxidant/oxidant status were determined in the cerebral cortex, hippocampus and striatum. Results: Hypothyroidism caused a marked upregulation in mRNA expression of catalase, superoxide dismutase (SOD-1, SOD-3), glutathione peroxidase (GPx-1, GPx-4) and thioredoxin reductase (TrxR-1) in brain structures. SOD-2 was increased in the cortex and striatum, while TrxR-2 increased in the cerebral cortex. The increase in mRNA expression of antioxidant enzymes was positively correlated with the Nrf-2 transcription in the cortex and hippocampus. Hypothyroidism caused oxidative stress, namely an increase in lipid peroxidation and reactive oxygen species levels in the hippocampus and striatum, and a decrease in nonprotein thiols in the cerebral cortex. Diphenyl diselenide was effective in reducing brain oxidative stress and normalizing most of the changes observed in gene expression of antioxidant enzymes. Conclusion: The present work corroborates and extends that hypothyroidism disrupts antioxidant enzyme gene expression and causes oxidative stress in the brain. Furthermore, diphenyl diselenide may be considered a promising molecule to counteract these effects in a hypothyroidism state.

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Regulation of cellular glutathione peroxidase by different forms and concentrations of selenium in primary cultured bovine hepatocytes

Cited by 32 publications

References 40 publications

Selenium Promotes T-Cell Response to TCR-Stimulation and ConA, but Not PHA in Primary Porcine Splenocytes

Selenium Promotes T-Cell Response to TCR-Stimulation and ConA, but Not PHA in Primary Porcine Splenocytes

Effect of selenium nanoparticles with different sizes in primary cultured intestinal epithelial cells of crucian carp, Carassius auratus gibelio

Diphenyl Diselenide Modulates Gene Expression of Antioxidant Enzymes in the Cerebral Cortex, Hippocampus and Striatum of Female Hypothyroid Rats

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