Effect of hydrogen peroxide on proliferation, apoptosis and interleukin-2 production of Jurkat T cells

• Published in: Biomedical sciences instrumentation Vol. 40; p. 123
• Main Authors: Nindl, Gabi, Peterson, Nathan R, Hughes, Ellen F, Waite, Lee R, Johnson, Mary T
• Format: Journal Article
• Language: English
• Published: United States 2004
• Subjects: Apoptosis - drug effects; Cell Division - drug effects; Dose-Response Relationship, Drug; Humans; Hydrogen Peroxide - pharmacology; Interleukin-2 - metabolism; Jurkat Cells - cytology; Jurkat Cells - drug effects; Jurkat Cells - physiology; Lymphocyte Activation - drug effects; Lymphocyte Activation - physiology
• ISSN: 0067-8856

Hydrogen peroxide (H2O2) is well known as a cell damaging agent that is produced during normal cell metabolism of aerobic organisms. An excessive production of oxygen metabolites such as H2O2 leads to oxidative stress and disease. On the other hand, it recently was discovered that H2O2 is not only a deleterious oxidant for cells but can also play an important role as a beneficial signaling molecule in certain cells such as T lymphocytes. T lymphocytes are major regulatory cells in the inflammatory cascade and can act by releasing either toxins or beneficial signaling molecules. Understanding how to regulate the actions of H2O2 in T cells will allow for the creation of novel ways to improve the treatment of inflammatory diseases. The current study presents baseline information on the effects of H2O2 on Jurkat cells, a T cell line that we use as a T cell model for therapeutic research. We first determined the half-life of 0-80 mumolar H2O2 added to Jurkat cultures using a realtime H2O2 monitoring system. We then exposed Jurkat cells to such H2O2 concentrations and found that 50 +/- 10 mumolar H2O2 promoted interleukin-2 production in cells activated with anti-CD3 at the T cell receptor plus phorbol myristate acetate as a co-stimulatory signal. These effects were not seen in non-activated, normal Jurkat cells, where H2O2 inhibited cell proliferation and induced apoptosis in a dose-dependent way without affecting interleukin-2 production. Our data indicate that Jurkat cells can model both healthy and inflammatory T cells that respond differently to oxidative metabolites such as H2O2.