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Journal of Environmental Pathology, Toxicology and Oncology
IF: 1.15 5-Year IF: 1.4 SJR: 0.519 SNIP: 0.613 CiteScore™: 1.61

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

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v26.i4.10
pages 245-254

Black Tea-Induced Amelioration of Hepatic Oxidative Stress through Antioxidative Activity in EAC-Bearing Mice

Arindam Bhattacharyya
Bose Institute, P-1/12 CIT Scheme VII M, Kolkata−700 054, India
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
Sankar 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
Uttam K. Ghosh
Bose Institute, P-1/12 CIT Scheme VII M, Kolkata−700 054, 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

ABSTRACT

It is recognized that during cancer, the disease itself as well as many of the anticancer drugs in use produce undesirable side effects such as hepatotoxicity. We have already demonstrated the antitumor and immunorestoring effects of black tea. Here we report Ehrlich's ascites carcinoma (EAC)—induced hepatotoxicity and its protection by antitumor dose of black tea in mice. Hepatotoxicity was adjudged by liver histopathology and by measurement of plasma level of alkaline phosphatase (ALP). An attempt to delineate the underlying mechanisms revealed tumor-induced generation of reactive oxygen species (ROS) on one hand and depression in antioxidants that neutralize ROS, i.e., superoxide dismutase (SOD), catalase, reduced glutathione (GSH), and glutathione-S-transferase (GST), on the other. As a result, lipid peroxidation, which leads to damage of host cell components, was increased. Treatment with antitumor dose of black tea could replenish the host's antioxidant system and regress cancer-induced ROS significantly, thereby protecting the host's liver from lipid peroxidation and subsequent degeneration. Thus, unlike many other anticancer agents, black tea not only has antitumor and immunorestoring properties, but it also protects host liver from tumor-induced toxicity. These results thus raise the possibility of inclusion of black tea in a successful therapeutic regimen against cancer.