detoxifiant enzyme seleno-glutathioneperoxidase-1
(GPx-1). We report a 30% decreased activity of the
chymotrypsin-like activity in cells overexpressing
GPx-1. This phenomenon correlated with a 2-fold in-
crease in IB half-life, a protein whose basal
turnover is 20S proteasome-dependent. Following
exposure to H2O2, these cells showed a seleno-de-
pendently decreased accumulation of intracellular re-
active oxygen species and 20S proteasome chy-
motrypsin-like activity. Similar results were obtained
in HeLa cells transiently overexpressing human GPx-
could be extracted
from thyroidal colloid by incubation with 0.5% sodium
dodecyl sulfate indicating that this enzyme is (i) secreted
into the follicular lumen and (ii) loosely attached to the
colloidal thyroglobulin. These findings are consistent with
a role of selenoproteins in the protection of the thyroid
from possible damage by H2O2. Particularly, GPx3 might
use excess H2O2 and catalyze the polymerization of
thyroglobulin to the highly cross-linked storage form
present in the colloid.
Keywords: deiodinase; glutathioneperoxidase1;
glutathione peroxidase 3
assessed in 52
CD patients and 99 volunteers and referred to clinical activity,
infl ammation, nutritional and antioxidant status.
Results: MDA/TBARS were higher in CD while oxLDL and
PP decreased in active disease and ROOH and OLAB did not
differ. oxLDL and PP negatively and OLAB positively cor-
related with CD activity. MDA/TBARS positively correlated
with IL-6 and SOD-1 and negatively with catalase. IL-6 and
SOD-1 explained 24 % in MDA/TBARS variability. PP nega-
tively correlated with CRP, platelets, and IL-6 and positively
predisposition and severity and accel-
erates recovery in a variety of pathologies. Pre-supple-
mentation Se levels and sex represent important
determinants of these Se-dependent health effects.
Accordingly, we previously reported on sexually dimor-
phic expression patterns of Se-dependent glutathioneperoxidase1, type I deiodinase, and selenoprotein P in
young mice. In the present study we investigated wheth-
er these differences vary with age. The strong sexual
dimorphic expression of hepatic type I deiodinase that
was observed in young mice vanished both at the mRNA
human trabecular meshwork cells. Invest Ophthalmol Vis Sci 2004; 45: 473-9. 14. Sacca SC, Izzotti A, Rossi P, et al. Glaucomatous outflow pathway and oxidative stress. Exp Eye Res 2007; 84: 389-99. 15. Prathima, Sindhu, Beena Shetty, Sadha K, Gayathri Rao. Role of redox methods, oxidative protein products and antioxidant potentials of thiols in diabetic retinopathy. Journal of Medical Biochemistry 2012; 31: 126-30. 16. Najafi M, Ghasemi H, Roustazadeh A, Alipoor B. Phe no - type and genotype relationship of glutathioneperoxidase1 (GPx1) and rs 1800668 variant: the
arteries. Glutathioneperoxidase-1 (GPX1), prevents oxida-
tive damage by detoxifying hydrogen and lipid peroxides.
GPX1 Pro198Leu polymorphism results in oxidant/antiox-
idant imbalance. 8-oxoguanine DNA glycosylase-1 (OGG1)
is the key enzyme in DNA repair pathway. OGG1 Ser326Cys
polymorphism leads to 8-oxoG accumulation and may
play a role in cardiovascular diseases. Thus, our study
aims to investigate GPX1 Pro198Leu and OGG1 Ser326Cys
polymorphisms in CAD patients and the possible relation-
ship of genotypes with serum lipids and CAD severity.
Objective: The aim of the current study was to investigate possible associations between catalase C262T (CAT C262T), glutathione peroxidase 1 Pro198Leu (GPX1 Pro198Leu), manganese superoxide dismutase Ala16Val (MnSOD Ala16Val) gene polymorphisms and non-Hodgkin Lymphoma risk (NHL) in a Romanian population and the five-year overall survival rate of the NHL patients.
Methods: We included in this case-control study 406 individuals, divided into two groups: the control group (n=315) and the patients group (n=91). The DNA was extracted from peripheral blood and amplified using specific techniques.
Results: The variant homozygous genotype of GPX1 Pro198Leu represents a risk factor for NHL development and no associations regarding the risk for NHL were found for MnSOD Ala16Val and CAT C262T gene polymorphisms. Two of the studied polymorphisms were associated with the overall survival rate thus: negative association regarding MnSOD Ala16Val, associated with higher overall survival rate and a positive one regarding CAT C262T, associated with lower overall survival rate.
Conclusions: According to our results, the mentioned polymorphisms may be considered as susceptible markers of the five-year overall survival rate for NHL patients. Future studies with a larger number of patients are needed to confirm our results.
inhibition of reactive oxygen species and activation of AMP-activated protein kinase. Microcirculation doi: 10.1111/j.1549-8719.2012.00186.x. 2012. 15. Felice F, Lucchesi D, di Stefano R, Barsotti MC, Storti E, Penno G, Balbarini A, Del Prato S, Pucci L. Oxidative stress in response to high glucose levels in endothelial cells and in endothelial progenitor cells: evidence for differential glutathioneperoxidase-1 expression. Microvasc Res 80(3): 332-8, 2010. 16. Pellegatta F, Bragheri M, Grigore L, Raselli S, Maggi FM, Brambilla C, Reduzzi A, Pirillo A, Norata GD
krmení hospodářských zvířat (Nutrition and feeding of livestock). Praha, Czech Republic, Profi Press, 360 pp. Zhang Y., ZhuS., Wang X., Wang CH., Li F. (2011). The effect of dietary selenium levels on growth performance, antioxidant capacity and glutathioneperoxidase1 (GSHPx1) mRNA expression in growing meat rabbits. Anim. Feed Sci. Technol., 169: 259-264.
of protein-dye binding, Anal. Biochem. 72 (1976) 248-254; DOI: 10.1016/0003-2697(76)90527-3. 16. A. Molaei Rad, H. Ghourchian, A. A. Moosavi-Movahedi, J. Hong and K. Nazari, Spectrophotometric assay for horseradish peroxidase activity based on pyrocatechol-aniline coupling hydrogen donor, Anal. Biochem. 362 (2007) 38-43; DOI: 10.1016/j.ab.2006.11.035. 17. D. E. Handy, E. Lu bos, Y. Yang, J. D. Galbraith, N. Kelly, Y. Y. Zhang, J. A. Leopold and J. Loscalzo, Glutathioneperoxidase-1 regulates mitochondrial function to modulate redox-dependent cellular responses, J