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Journal of Environmental Pathology, Toxicology and Oncology
IF: 1.241 5-Year IF: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvPathToxOncol.v24.i2.30
pages 91-104

Black Tea Protects Thymocytes in Tumor-Bearing Animals by Differential Regulation of Intracellular ROS in Tumor Cells and Thymocytes

Deba Prasad Mandal
Department of Zoology, West Bengal State University, Berunanpukuria, Malikapur, North-24 Parganas, Barasat, Kolkata-700126, West Bengal, India
Lakshmishri Lahiry
Bose Institute, P-1/12 CIT Scheme VII M, Kolkata−700 054, India
Arindam Bhattacharyya
Bose Institute, P-1/12 CIT Scheme VII M, Kolkata−700 054, India
Sreya Chattopadhyay
Bose Institute, P-1/12 CIT Scheme VII M, Kolkata−700 054, India
Maqsood Siddiqi
Department of Environmental Carcinogenesis and Toxicology, Chittaranjan National Cancer Institute; and Bose Institute, Calcutta, India
Gaurisankar Sa
Bose Institute, P-1/12 CIT Scheme VII M, Kolkata−700 054, India
Tanya Das
Bose Institute, P-1/12 CIT Scheme VII M, Kolkata−700 054, India


The accumulated in vitro evidence indicates that many tumors induce T-cell apoptosis as a mechanism of inhibiting antitumor activity. This downregulation of cell-mediated immune functions occurring at the late stages of the disease may be causally related to the thymic involution, because the thymus is the major site of T-cell maturation, extensive proliferation, and differentiation. Our results showed that in Erhlich's ascites carcinoma cell (EAC)-bearing mice, the number of EAC was inversely proportional to the thymocyte count in the host's thymus, which is the primary immune organ. Further studies indicated the presence of tumor-induced thymocyte apoptosis in EAC bearers. Black tea prolonged the survival of the tumor bearer by successfully restricting tumor progression as well as protecting the thymus from tumor insult. In fact, black tea inhibited thymic apoptosis while inducing programmed cell death of EAC. Interestingly, the tea regulated the oxidant status differentially in EAC and thymocytes—i.e., it reduced the EAC-induced reactive oxygen species (ROS) generation in the thymus while activating the same in the EAC. A similar effect of black tea was obtained when thymocytes were cultured in the presence of cell-free ascitic fluid, thereby indicating that black tea could directly reduce oxidative stress, an activity independent of its tumoricidal property. As a result, the maturation block in thymocyte subpopulations in tumor bearers was ameliorated significantly in black tea-treated animals. Our results demonstrate that black tea protects thymocytes in the tumor bearer by regulating the intracellular ROS in tumor cells and thymocytes differentially, thereby strengthening its candidacy in future anticancer therapeutic regimens.

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