title: Black tea protects thymocytes in tumor-bearing animals by differential regulation of intracellular ROS in tumor cells and thymocytes.
abstract: 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.
authors.affiliation: Bose Institute, Kolkata-700 054, India.
authors.forename: Debaprasad
authors.initials: D
authors.lastname: Mandal
authors.forename: Lakshmishri
authors.initials: L
authors.lastname: Lahiry
authors.forename: Arindam
authors.initials: A
authors.lastname: Bhattacharyya
authors.forename: Sreya
authors.initials: S
authors.lastname: Chattopadhyay
authors.forename: Maqsood
authors.initials: M
authors.lastname: Siddiqi
authors.forename: Gaurisankar
authors.initials: G
authors.lastname: Sa
authors.forename: Tanya
authors.initials: T
authors.lastname: Das
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D028241:Camellia sinensis; D002286:Carcinoma, Ehrlich Tumor / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D002452:Cell Count; D002453:Cell Cycle; D045744:Cell Line, Tumor; D002470:Cell Survival; D051379:Mice; D009368:Neoplasm Transplantation; D010936:Plant Extracts / Q000494:pharmacology; D011003:Ploidies; D017382:Reactive Oxygen Species / Q000378:metabolism*; D016176:T-Lymphocyte Subsets / Q000187:drug effects; D013601:T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D013662:Tea; D013950:Thymus Gland / Q000378:metabolism
chemical_list: D016588:Anticarcinogenic Agents; D000975:Antioxidants; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D013662:Tea