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The Role of Redox Status Changes in Dexamethasone-Induced Apoptosis in Jurkat Tumor Cells

О L Nosareva1, E A Stepovaya2, E V Shakhristova2

  • 1Siberian State Medical University, Ministry of Health of the Russian Federation, Tomsk, Russia. olnosareva@yandex.ru.

Bulletin of Experimental Biology and Medicine
|February 17, 2022
PubMed

Insights

Glutathione system blockage enhances dexamethasone-induced apoptosis in Jurkat cells by affecting TNF RI and Fas receptors. Decreased oxidized glutathione potentiates this cell death pathway.

Area of Science:

  • Cell Biology
  • Biochemistry
  • Immunology

Background:

  • Apoptosis, or programmed cell death, is crucial for multicellular organisms.
  • The role of the glutathione system in regulating apoptosis is not fully understood.
  • Jurkat cells are a human T-cell leukemia line commonly used in apoptosis research.

Purpose of the Study:

  • To investigate the role of glutathione system components in dexamethasone-induced apoptosis in Jurkat cells.
  • To analyze how glutathione synthesis inhibition affects apoptosis signaling pathways.
  • To determine the impact of oxidized glutathione levels on programmed cell death.

Main Methods:

  • Jurkat cells were treated with buthionine-sulfoximine (glutathione synthesis inhibitor) and/or dexamethasone (apoptosis inducer).
  • Analysis of receptor-mediated (TNF RI, Fas) and mitochondrial apoptosis pathways.
  • Quantification of transcription factors Apaf-1 and NF-κB.
  • Measurement of oxidized glutathione levels.

Main Results:

  • Glutathione system blockage significantly affected the presentation of TNF Receptor 1 (TNF RI) and Fas receptors in dexamethasone-treated Jurkat cells.
  • Inhibition of glutathione synthesis altered the content of transcription factors Apaf-1 and NF-κB, promoting cell death.
  • A decrease in oxidized glutathione levels potentiated dexamethasone-induced apoptotic cell death.

Conclusions:

  • The glutathione system plays a critical role in regulating dexamethasone-induced apoptosis in Jurkat cells.
  • Modulating glutathione levels, particularly reducing oxidized glutathione, can enhance programmed cell death.
  • Targeting the glutathione system may offer therapeutic strategies for T-cell malignancies.
Keywords:
Jurkat tumor cellsapoptosisbuthioninesulfoximinedexamethasoneglutathione system

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