The impact of catalase and glutathione peroxidase‐1 genetic polymorphisms on their enzyme activities among Egyptian patients with keratoconus

2020 ◽  
Vol 22 (8) ◽  
Author(s):  
Rehab S. Abdul‐Maksoud ◽  
Rania A. Fouad ◽  
Tamer G. Elsayed ◽  
Reda A. Ibrahem ◽  
Amani E. Badawi
2020 ◽  
Author(s):  
Xiaojun Shao ◽  
Dongxue Sun ◽  
Bihui Zhang ◽  
Lingfei Cheng ◽  
Ci Yan ◽  
...  

Abstract Purpose: Glutathione Peroxidase 1 (GPx1) is the most abundantly expressed of the glutathione peroxidase (GPx) family. The impact of GPx1 polymorphisms has been rarely explored in the field of personality traits. Therefore, we analyzed relationships between GPx-1 polymorphisms and personality traits in healthy Chinese-Han subjects. Methods: 493 Chinese-Han participants (male=234, female=259) were recruited. Personality traits were assessed by Tridimensional Personality Questionnaire (TPQ). GPx-1 gene polymorphisms were detected through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).Results: The results indicated that the GPx-1 polymorphisms rs1050450 and rs1800668 were associated with the personality trait novelty seeking (NS). Our data found a correlation between rs1800668 and NS2 (X2=7.392, P=0.025). While the results showed the rs1050450 was significantly associated with NS4 (X2=6.059, P=0.048). Regarding sex stratification, there was a significant difference in the NS2 score (X2=8.232, P=0.016) among women for rs1800668. There was no difference in TPQ scores among the different genotypic groups in males. Additionally, no sex effect was observed for either genotype for rs1050450. Conclusion: Our results suggested that GPx-1 may be a potential gene that influenced personality.


2007 ◽  
pp. 50-53
Author(s):  
M. A. Solodilova ◽  
V. P. Ivanov ◽  
A. V. Polonikov ◽  
I. V. Khoroshaya ◽  
M. A. Kozhukhov ◽  
...  

Author(s):  
Sunmi Lee ◽  
Eun-Kyung Lee ◽  
Dong Hoon Kang ◽  
Jiyoung Lee ◽  
Soo Hyun Hong ◽  
...  

AbstractGlutathione peroxidase (GPx) is a selenocysteine-containing peroxidase enzyme that defends mammalian cells against oxidative stress, but the role of GPx signaling is poorly characterized. Here, we show that GPx type 1 (GPx1) plays a key regulatory role in the apoptosis signaling pathway. The absence of GPx1 augmented TNF-α-induced apoptosis in various RIPK3-negative cancer cells by markedly elevating the level of cytosolic H2O2, which is derived from mitochondria. At the molecular level, the absence of GPx1 led to the strengthened sequential activation of sustained JNK and caspase-8 expression. Two signaling mechanisms are involved in the GPx1-dependent regulation of the apoptosis pathway: (1) GPx1 regulates the level of cytosolic H2O2 that oxidizes the redox protein thioredoxin 1, blocking ASK1 activation, and (2) GPx1 interacts with TRAF2 and interferes with the formation of the active ASK1 complex. Inducible knockdown of GPx1 expression impaired the tumorigenic growth of MDA-MB-231 cells (>70% reduction, P = 0.0034) implanted in mice by promoting apoptosis in vivo. Overall, this study reveals the apoptosis-related signaling function of a GPx family enzyme highly conserved in aerobic organisms.


Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 529
Author(s):  
Silvia Selene Moreno-Guerrero ◽  
Arturo Ramírez-Pacheco ◽  
Luz María Rocha-Ramírez ◽  
Gabriela Hernández-Pliego ◽  
Pilar Eguía-Aguilar ◽  
...  

There is evidence that high circulating levels of IL-6 and IL-8 are markers of a poor prognosis in various types of cancer, including NB. The participation of these cytokines in the tumor microenvironment has been described to promote progression and metastasis. Our objective was to evaluate the prognostic role of genetic polymorphisms and serum levels of IL-6 and IL-8 in a cohort of Mexican pediatric patients with NB. The detection of the SNPs rs1800795 IL-6 and rs4073 and rs2227306 IL-8 was carried out by PCR-RFLP and the levels of cytokines were determined by the ELISA method. We found elevated circulating levels of IL-8 and IL-6 in NB patients compared to the control group. The genotype frequencies of the rs1800795 IL-6 and rs4073 IL-8 variants were different between the patients with NB and the control group. Likewise, the survival analysis showed that the GG genotypes of rs1800795 IL-6 (p = 0.014) and AA genotypes of rs4073 IL-8 (p = 0.002), as well as high levels of IL-6 (p = 0.009) and IL-8 (p = 0.046), were associated with lower overall survival. We confirmed the impact on an adverse prognosis in a multivariate model. This study suggests that the SNPs rs1800795 IL-6 and rs4073 IL-8 and their serum levels could be promising biomarkers of a poor prognosis, associated with overall survival, metastasis, and a high risk in Mexican children with NB.


2021 ◽  
Vol 27 (Supplement_1) ◽  
pp. S27-S27
Author(s):  
Jared Hendren ◽  
Koral Kasnyik ◽  
Christopher Williams ◽  
Sarah Short

Abstract Many selenium-containing “selenoproteins” function as antioxidants, and work by our lab and others has demonstrated that selenoproteins often protect against intestinal inflammatory diseases, including colitis. Glutathione peroxidase 1 (GPx1) is a ubiquitous, mitochondrial and cytosolic selenoprotein which catalyzes the reduction of hydrogen peroxide by glutathione. Previously, we determined that despite its antioxidant role, loss of GPx1 greatly reduced disease severity in the dextran sodium sulfate (DSS) colitis model. Furthermore, GPx1 loss increased baseline intestinal cell proliferation, enhanced enteroid plating efficiency, and induced expression of stem cell-associated genes, such as Lgr5. Next, we aimed to determine the mechanism by which GPx1 modifies response to DSS. We observed that GPx1 is increased in colonic tissues from DSS-treated mice as compared to nontreated controls, suggesting that GPx1 may functionally contribute to intestinal injury responses. While GPx1 is expressed in both intestinal epithelial and immune cells, in situ hybridization to visualize Gpx1 identified epithelial cells as the most highly expressing cell type, with the greatest Gpx1 upregulation observed in wound-adjacent and regenerative crypts. Next, we investigated whether GPx1 loss affects stem cell function after injury. Here, we determined that both proliferation (p<0.01) and Lgr5 expression (p<0.05) were increased in the crypts of Gpx1-/- DSS-treated mice in comparison to WT controls. Similarly, organoids established from ulcerative colitis tissue displayed increased growth rates (p<0.01), expression of stem cell and Wnt target genes such as AXIN2 (p<0.0001) and LGR5 (p<0.01), and proliferation (p<0.05) following GPX1 knockdown. Together, these results indicate that GPx1 has an epithelial-cell autonomous role, and that its loss activates stem cell and proliferative responses which may both protect from intestinal injury and promote healing. Interestingly, recent research has highlighted the role of cellular metabolism in maintaining intestinal stem cell function, and GPx1 has previously been implicated in these processes. RNA-sequencing from DSS-treated mice and gene set enrichment analysis identified a positive association with oxidative phosphorylation-associated genes in Gpx1-/- mice (NES: 1.78; FDR q-val: 0.01), suggesting altered metabolism which may favor stem cell function. Further analysis of cellular metabolism using GPX1 knockdown colorectal cancer cells observed higher basal respiration (p<0.0001) and ATP generation (p<0.0001). Together, these results suggest that unlike other intestinal selenoproteins studied to date, loss of GPx1 augments stem cell injury responses to protect against intestinal inflammation, likely via augmenting epithelial regenerative responses.


2008 ◽  
Vol 179 (4S) ◽  
pp. 459-459
Author(s):  
Canan Kucukgergin ◽  
Oner Sanli ◽  
Tzevat Tefik ◽  
Ismet Nane ◽  
Sule Seckin ◽  
...  

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