IMR Press / FBE / Volume 5 / Issue 2 / DOI: 10.2741/E651

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

Thymoquinone induces apoptosis in malignant T-cells via generation of ROS

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1 Department of Biology, American University of Beirut, Beirut, Lebanon
2 Medical Laboratory Sciences Program, American University of Beirut, Beirut, Lebanon
3 Internal Medicine, American University of Beirut, Lebanon
4 Experimental Tumor Pathology, Institute for Pathology, University Erlangen-Nuremberg, Germany

*Author to whom correspondence should be addressed.

Academic Editor: Hala Gali-Muhtasib

Front. Biosci. (Elite Ed) 2013, 5(2), 706–719; https://doi.org/10.2741/E651
Published: 1 January 2013
(This article belongs to the Special Issue New emerging anticancer lead compounds from plants)
Abstract

We show that HTLV-1 negative leukemia cells are more sensitive to TQ due to higher levels of drug-induced reactive oxygen species (ROS). PreG1 population in HTLV-1 negative Jurkat and CEM was higher than HTLV-1 transformed HuT-102 and MT-2 cells. Peripheral blood mononuclear cells were more resistant. Hoechst staining indicated more features of apoptosis, namely nuclear blebs and shrunken nuclei in HuT-102 than Jurkat. A greater depletion of the antioxidant enzyme glutathione occurred in Jurkat, which consequently led to an increase in ROS, loss of mitochondrial membrane potential, cytochrome c release, activation of caspases 3 and 9, and cleavage of PARP. Treatment with z-VAD-fmk partially reversed TQ-induced apoptosis, suggesting a caspase-dependent mechanism. N-acetyl cysteine prevented apoptosis providing evidence that cell death is ROS- dependent. Catalase prevented apoptosis to a lesser extent than NAC. In summary, TQ induces apoptosis in adult T cell leukemia/lymphoma by decreasing glutathione and increasing ROS, and levels of ROS underlie the differential cellular response to TQ. Our data suggest a potential therapeutic role for TQ in sensitizing HTLV-I-negative T-cell lymphomas.

Keywords
T-cell leukemia
Thymoquinone
ROS
Apoptosis
Anticancer
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