Selective up-regulation of human selenoproteins in response to oxidative stress

Touat-Hamici, Zahia; Legrain, Yona; Bulteau, Anne‐Laure; Chavatte, Laurent

doi:10.1016/j.freeradbiomed.2014.10.745

Cited by 4 publications

(3 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Dietary Se deficiency and oxidative stress have been linked to selective regulation of several selenoproteins involved in antioxidant defense and redox homeostasis [87,88], and such regulation is believed to be tissue-specific [12,89]. Indeed, in the current study, the expression of Gpx1, Gpx3, and Gpx4 was differentially regulated in ovaries of aging mice.…”

Section: Expression Of Gpx1 Gpx3 Gpx4 Selenof Bcl-2 and P21mentioning

confidence: 55%

Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice

et al. 2019

View full text Add to dashboard Cite

Female reproductive (ovarian) aging is distinctively characterized by a markedly reduced reproductive function due to a remarkable decline in quality and quantity of follicles and oocytes. Selenium (Se) has been implicated in playing many important biological roles in male fertility and reproduction; however, its potential roles in female reproduction, particularly in aging subjects, remain poorly elucidated. Therefore, in the current study we used a murine model of female reproductive aging and elucidated how different Se-levels might affect the reproductive efficiency in aging females. Our results showed that at the end of an 8-week dietary trial, whole-blood Se concentration and blood total antioxidant capacity (TAOC) were significantly reduced in Se-deficient (0.08 mg Se/kg; Se-D) mice, whereas both of these biomarkers were significantly higher in inorganic (0.33 mg/kg; ISe-S) and organic (0.33 mg/kg; OSe-S) Se-supplemented groups. Similarly, compared to the Se-D group, Se supplementation significantly ameliorated the maintenance of follicles and reduced the rate of apoptosis in ovaries. Meanwhile, the rate of in vitro-produced embryos resulting from germinal vesicle (GV) oocytes was also significantly improved in Se-supplemented (ISe-S and OSe-S) groups compared to the Se-D mice, in which none of the embryos developed to the hatched blastocyst stage. RT-qPCR results revealed that mRNA expression of Gpx1, Gpx3, Gpx4, Selenof, p21, and Bcl-2 genes in ovaries of aging mice was differentially modulated by dietary Se levels. A considerably higher mRNA expression of Gpx1, Gpx3, Gpx4, and Selenof was observed in Se-supplemented groups compared to the Se-D group. Similarly, mRNA expression of Bcl-2 and p21 was significantly lower in Se-supplemented groups. Immunohistochemical assay also revealed a significantly higher expression of GPX4 in Se-supplemented mice. Our results reasonably indicate that Se deficiency (or marginal levels) can negatively impact the fertility and reproduction in females, particularly those of an advancing age, and that the Se supplementation (inorganic and organic) can substantiate ovarian function and overall reproductive efficiency in aging females.

show abstract

Section: Expression Of Gpx1 Gpx3 Gpx4 Selenof Bcl-2 and P21mentioning

confidence: 55%

Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Sec, a stop signal in translation, is built in by the ribosome using a UGA codon. The 3′ untranslated regions (UTRs) of selenoprotein mRNAs contain a secondary structure called the Sec insertion sequence (SECIS) element, which controls the UGA to keep off the formation of truncated proteins so that it can prevent premature translational termination [ 29 , 30 , 31 , 32 , 33 , 34 ]. A later study revealed that the interaction between SECIS and SECIS binding protein 2 (SBP2) is a vital nodal point for the metabolic balance between selenium and selenoproteins, and GPX4 has specific binding appeal to SBP2 in cells [ 35 ].…”

Section: Regulation Of Gpx4 Expressionmentioning

confidence: 99%

Prospects for Anti-Tumor Mechanism and Potential Clinical Application Based on Glutathione Peroxidase 4 Mediated Ferroptosis

Chen

Shi

Sun

et al. 2023

IJMS

View full text Add to dashboard Cite

Ferroptosis, characterized by excessive iron accumulation and lipid peroxidation, is a novel form of iron-dependent cell death, which is morphologically, genetically, and biochemically distinct from other known cell death types, such as apoptosis, necrosis, and autophagy. Emerging evidence shows that glutathione peroxidase 4 (GPX4), a critical core regulator of ferroptosis, plays an essential role in protecting cells from ferroptosis by removing the product of iron-dependent lipid peroxidation. The fast-growing studies on ferroptosis in cancer have boosted a perspective on its use in cancer therapeutics. In addition, significant progress has been made in researching and developing tumor therapeutic drugs targeting GPX4 based on ferroptosis, especially in acquired drug resistance. Selenium modulates GPX4-mediated ferroptosis, and its existing form, selenocysteine (Sec), is the active center of GPX4. This review explored the structure and function of GPX4, with the overarching goal of revealing its mechanism and potential application in tumor therapy through regulating ferroptosis. A deeper understanding of the mechanism and application of GPX4-mediated ferroptosis in cancer therapy will provide new strategies for the research and development of antitumor drugs.

show abstract

“…Failure to incorporate Sec diminishes the catalytic prowess of selenoenzymes [6–14] and compromises the structure of selenoproteins, and introduction of Sec improves function of artificial selenoenzymes and confers resistance to inactivation by oxidation (reviewed in [5]). Consistent with its redox and antioxidant function, levels of many selenoprotein genes and selenoproteins are significantly increased under oxidative stress [15,16]. Disruption or deletion of genes encoding selenocysteine tRNA (tRNA Sec ), glutathione peroxidase 4 (GPx4), and thioredoxin reductase 1 (Trx1) and 3 (Trx3) causes embryonically lethal phenotypes in mice, accentuating the significance of maintaining selenoproteome integrity [17–20].…”

Section: Introductionmentioning

confidence: 99%

On elongation factor eEFSec, its role and mechanism during selenium incorporation into nascent selenoproteins

Simonović

Puppala

2018

Biochimica et Biophysica Acta (BBA) - General Subjects

View full text Add to dashboard Cite

Based on current findings, a non-canonical mechanism for elongation of selenoprotein synthesis at the Sec UGA codon is proposed. Although incomplete, our understanding of this fundamental biological process is significantly improved, and it is being harnessed for biomedical and synthetic biology initiatives. This article is part of a Special Issue entitled "Selenium research" in celebration of 200 years of selenium discovery, edited by Dr. Elias Arnér and Dr. Regina Brigelius-Flohe.

show abstract

Selective up-regulation of human selenoproteins in response to oxidative stress

Cited by 4 publications

References 23 publications

Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice

Dietary Selenium Supplementation Ameliorates Female Reproductive Efficiency in Aging Mice

Prospects for Anti-Tumor Mechanism and Potential Clinical Application Based on Glutathione Peroxidase 4 Mediated Ferroptosis

On elongation factor eEFSec, its role and mechanism during selenium incorporation into nascent selenoproteins

Contact Info

Product

Resources

About