Human GPX1 blocking peptide

The objective of the study was to examine the effects of different doses of dietary organic selenium (Se) on humoral immune response, hepatic antioxidant status, mRNA expression of key selenoproteins and oxidative stability of lamb meat. Twenty lambs aging 5-6 months received during a 90-day period a basal diet unsupplemented or supplemented with 0.5, 1.5 or 4.5 ppm Se (selenized yeasts). After experimental period, immune response against Peste des petits ruminants (PPR) virus vaccine, hepatic antioxidant status, selenoproteins gene expression, histology of liver, kidney, spleen and thymus, and meat oxidative stability after 0, 3, 7 and 10 days of storage were studied. Significantly higher serum PPR antibody titre and hepatic total antioxidant capacity in lambs fed diet supplemented with 1.5 and 4.5 ppm Se were shown. Gene expression of glutathione peroxidase 1 (GPX1) and GPX3 was increased in group with 0.5 ppm Se supplementation. While selenoprotein 15 and iodothyronine deiodinase 1 (DIO1) mRNA levels were not influenced by supranutritional Se supplementation, DIO3 mRNA level was upregulated at 4.5 ppm Se addition. Selenoprotein P and W1 gene expression were significantly upregulated by 1.5 and 4.5 ppm Se supplementation, respectively. Thioredoxin reductase 1 gene expression was decreased by 4.5 ppm Se. No appreciable dfferences in meat lipid oxidation were observed amongst treatments. So, feeding 1.5 ppm organic Se could be beneficial in improving humoral immune response to PPR vaccine and hepatic antioxidant status in lambs. Further, the expression of genes encoding selenoproteinases depends on their type and dose of Se in the diet. The studied Se doses did not induce toxicity in organs but exhibited limited potential to enhance meat oxidative stability.

Altered redox state modulates the expression levels of endothelial K(Ca)2.3 and K(Ca)3.1 (K(Ca)s) in normal pregnancy (NP) and preeclampsia (PE), thereby regulating vascular contractility. The mechanisms underlying K(Ca)s endocytosis and transportation remain unknown. We investigated the regulation of K(Ca)s expression in plasma membrane (PM) during NP and PE. Cultured human uterine artery endothelial cells were incubated in serum from normal nonpregnant women and women with NP or PE, or in oxidized LDL-, or lysophosphatidylcholine- (LPC-) containing a medium for 24 hours. NP serum elevated PM levels of K(Ca)s and reduced caveolin-1 and clathrin levels. PE serum, oxidized LDL, or LPC reduced PM levels of K(Ca)s and elevated caveolin-1, clathrin, Rab5c, and early endosome antigen-1 (EEA1) levels. Reduced K(Ca)s levels by PE serum or LPC were reversed by inhibition of caveolin-1, clathrin, or EEA1. Catalase and glutathione peroxidase 1 (GPX1) knockdown elevated PM-localized K(Ca)s levels and reduced caveolin-1 and clathrin levels. Elevated K(Ca)2.3 levels upon catalase and GPX1 knockdown were reversed by PEG-catalase treatment. An H2O2 donor reduced clathrin and Rab5c. In contrast, elevated clathrin, caveolin-1, or colocalization of caveolin-1 with K(Ca)3.1 by PE serum or LPC was reversed by NADPH oxidase inhibitors or antioxidants. A superoxide donor xanthine+xanthine oxidase elevated caveolin-1 or Rab5c levels. We concluded that K(Ca)s are endocytosed in a caveola- or a clathrin-dependent manner and transported in a Rab5c- and EEA1-dependent manner during pregnancy. The endocytosis and transportation processes may slow down via H2O2-mediated pathways in NP and may be accelerated via superoxide-mediated pathways in PE.