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Selenoproteins and the senescence-associated epitranscriptome.

May Y Lee1,2, Stephen Ojeda-Britez1, Dylan Ehrbar2,3,4

  • 1College of Nanoscale Science and Engineering, SUNY Polytechnic Institute, Albany, NY 12203, USA.

Experimental Biology and Medicine (Maywood, N.J.)
|August 29, 2022
PubMed
Summary

Selenium and its vital selenoproteins are crucial for antioxidant defense and healthy aging. This review explores how regulating selenoprotein synthesis, via epitranscriptomic marks, may impact cellular senescence and age-related diseases.

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RNA modificationsSASPSenescenceseleniumselenoproteins

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Area of Science:

  • Biochemistry and Molecular Biology
  • Cellular Senescence
  • Epigenetics and Epitranscriptomics

Background:

  • Selenium is an essential trace element with antioxidant, anticancer, and immune-boosting properties.
  • Selenoproteins, incorporating the 21st amino acid selenocysteine, are key for redox homeostasis and antioxidant defense.
  • Selenocysteine incorporation involves a unique UGA stop codon recoding mechanism.

Purpose of the Study:

  • To investigate the role of upstream events regulating selenoprotein synthesis in senescence-associated pathologies.
  • To explore the connection between epitranscriptomic marks, selenocysteine utilization, and the cellular senescence program.

Main Methods:

  • Review of existing literature on selenium, selenoproteins, aging, and senescence.
  • Focus on the function of alkylation repair homolog 8 (ALKBH8) in selenoprotein production.
  • Analysis of the impact of ALKBH8 deficiency on reactive oxygen species (ROS) detoxification and oxidative stress.

Main Results:

  • ALKBH8 is critical for selenoprotein synthesis; its deficiency reduces selenoprotein levels.
  • Decreased selenoproteins lead to impaired ROS detoxification and increased oxidative stress.
  • Increased oxidative stress is a major driver of cellular senescence.

Conclusions:

  • Epitranscriptomic regulation of selenocysteine incorporation may play a significant role in cellular senescence.
  • Dysregulation of selenoprotein synthesis due to impaired epitranscriptomic marks could contribute to senescence-associated pathologies.
  • Further research into epitranscriptomic marks governing selenoprotein synthesis is warranted to understand aging and related diseases.