AI Article Synopsis

  • Selenium (Se) is vital for selenoproteins and helps regulate enzymes involved in redox signaling, influencing antioxidant activities.
  • Se compounds show potential in protecting against radiation-induced damage, making them promising candidates for new radioprotective agents in cancer treatment.
  • The review focuses on how these seleno-compounds enhance cellular stress responses, particularly through Nrf2 modulation, to mitigate radiation toxicity in critical tissues like bone marrow.

Article Abstract

The trace element selenium (Se) is an essential component of selenoproteins and plays a critical role in redox signaling via regulating the activity of selenoenzymes such as thioredoxin reductase-1 and glutathione peroxidases. Se compounds and its metabolites possess a wide range of biological functions including anticancer and cytoprotection effects, modulation of hormetic genes and antioxidant enzyme activities. Radiation-induced injury of normal tissues is a significant side effect for cancer patients who receive radiotherapy in the clinic and the development of new and effective radioprotectors is an important goal of research. Others and we have shown that seleno-compounds have the potential to protect ionizing radiation-induced toxicities in various tissues and cells both in in vitro and in vivo studies. In this review, we discuss the potential utilization of Se compounds with redox-dependent hormetic activity as novel radio-protective agents to alleviate radiation toxicity. The cellular and molecular mechanisms underlying the radioprotection effects of these seleno-hormetic agents are also discussed. These include Nrf2 transcription factor modulation and the consequent upregulation of the adaptive stress response to IR in bone marrow stem cells and hematopoietic precursors.

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http://dx.doi.org/10.1002/biof.1578DOI Listing

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Article Synopsis
  • Selenium (Se) is vital for selenoproteins and helps regulate enzymes involved in redox signaling, influencing antioxidant activities.
  • Se compounds show potential in protecting against radiation-induced damage, making them promising candidates for new radioprotective agents in cancer treatment.
  • The review focuses on how these seleno-compounds enhance cellular stress responses, particularly through Nrf2 modulation, to mitigate radiation toxicity in critical tissues like bone marrow.
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2,2'-diselenyldibenzoic acid (DSBA) is a chemical probe produced to explore the pharmacological properties of diphenyldiselenide-derived agents with seleno-hormetic activity undergoing preclinical development. The present study was designed to verify in vivo the drug's properties and to determine mechanistically how these may mediate the protection of tissues against stress conditions, exemplified by ionizing radiation induced damage in mouse bone marrow. In murine bone marrow hematopoietic cells, the drug initiated the activation of the Nrf2 transcription factor resulting in enhanced expression of downstream stress response genes.

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