Black tea-induced amelioration of hepatic oxidative stress through antioxidative activity in EAC-bearing mice.

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.