The production of reactive oxygen species enhanced with the reduction of menadione by active thioredoxin reductase.

  title={The production of reactive oxygen species enhanced with the reduction of menadione by active thioredoxin reductase.},
  author={Jing Li and Xin Zuo and Ping Cheng and Xiaoyuan Ren and Shibo Sun and Jianqiang Xu and Arne Holmgren and Jun Lu},
  journal={Metallomics : integrated biometal science},
  • Jing Li, Xin Zuo, Jun Lu
  • Published 18 September 2019
  • Biology
  • Metallomics : integrated biometal science
Cytosolic thioredoxin reductase (TXNRD1) is an important selenoprotein that participates in the reduction of thioredoxin and many other redox-related substrates. The enhancement of ROS production to cause cancer cell death is an effective anticancer strategy. Herein, we found that menadione substantially increased ROS generation via interaction with TXNRD1. To elucidate the mechanism behind this, various TXNRD1 mutant proteins were used to investigate the relationship between ROS production and… 
Chlorophyllin Inhibits Mammalian Thioredoxin Reductase 1 and Triggers Cancer Cell Death
Five out of 15 commercial food colorants, namely, lutein, betanin, caramel, crocin and chlorophyll, significantly inhibited wild type selenoprotein thioredoxin reductase 1 (TrxR1, TXNRD1) in vitro in vitro to contribute to understand the food safety of commercial colorants and provide chemotherapeutic compounds by targeting TrxR 1.
A non-canonical vitamin K cycle is a potent ferroptosis suppressor.
It is shown that the fully reduced forms of vitamin K-a group of naphthoquinones that includes menaquinone and phylloquinone3-confer a strong anti-ferroptotic function, in addition to the conventional function linked to blood clotting by acting as a cofactor for γ-glutamyl carboxylase.
Selenite Ameliorates Cadmium-induced Cytotoxicity Through Downregulation of ROS Levels and Upregulation of Selenoprotein Thioredoxin Reductase 1 in SH-SY5Y Cells.
Results showed that Se supplements attenuated the ROS production and apoptosis in SH-SY5Y cells, and significantly mitigated Cd-induced SH- SY5Y cell death, which may be helpful for understanding the therapeutic potential of Cd and Se in treating or preventing neurodegenerative diseases, like Alzheimer's disease and Parkinson's disease.
Menadione-induced endothelial inflammation detected by Raman spectroscopy.


Disruption of thioredoxin reductase 1 protects mice from acute acetaminophen-induced hepatotoxicity through enhanced NRF2 activity.
The results suggest that Txnrd1(ΔLiv) mice are primed for xenobiotic detoxication primarily through NRF2 activation.
Thioredoxin 1 Is Inactivated Due to Oxidation Induced by Peroxiredoxin under Oxidative Stress and Reactivated by the Glutaredoxin System*
Background: The Cys-62/Cys-69 dithiol of Trx1 is predicted to have a profound effect on cell signaling. Results: The Cys-62/Cys-69 dithiol of Trx1 was oxidized by Prx1, and this disulfide was reduced
The thioredoxin system in cancer.
Glutathione and Glutaredoxin Act as a Backup of Human Thioredoxin Reductase 1 to Reduce Thioredoxin 1 Preventing Cell Death by Aurothioglucose*
The glutaredoxin system and glutathione have a backup role to keep Trx1 reduced in cells with loss of TrxR1 activity, and this work demonstrated the critical role of the thioredoxin redox state in cell survival and a new role of glutATHione.
The conserved Trp114 residue of thioredoxin reductase 1 has a redox sensor-like function triggering oligomerization and crosslinking upon oxidative stress related to cell death
The results collectively suggest that Trp114 of TrxR1 serves a function reminiscent of an irreversible sensor for excessive oxidation, thereby presenting a previously unrecognized level of regulation of TrXR1 function in relation to cellular redox state and cell death induction.
Thioredoxin system in cell death progression.
This work focuses on the research progress that is involved in the regulation of apoptosis by Trx systems, and proposes some useful principles to understand the reaction mechanism of the TrxR inhibition by these compounds.