title: Antioxidant potential of black tea against 7,12-dimethylbenz(a)anthracene- induced oxidative stress in Swiss albino mice.
abstract: Oxygen free radicals and related reactive species have been implicated in the etiology of many diseases, such as atherosclerosis, neurodegenerative disorders, and cancer. Antioxidant enzymes exist in cells to protect against the effects of these free radicals and other oxygen-derived species, which are produced during the oxidative stress. Tea (Camellia sinensis) is the most commonly consumed beverage worldwide. Both green and black tea are known to possess many pharmacological properties, including antioxidant, antipyretic, antibacterial, and antineoplastic effects. In the present study, the preventive effects of black tea extract (BTE) was evaluated in Swiss albino mice against 7,12-dimethyl benz(a)anthracene (DMBA)-induced oxidative stress. The animals were given 0.5%, 1%, and 1.5% BTE as the sole source of drinking solution for 1 week prior to the administration of DMBA, which was given orally as a single dose of 50 mg/kg body weight. At the end of the study period, the liver, kidney, and prostate tissues were dissected out for the determination of antioxidant enzyme levels (catalase, superoxide dismutase, glutathione reductase, glutathione-S-transferase), and lipid peroxidation. A dose-dependent protective effect of BTE against DMBA-induced depletion in enzymes activity was observed in all three tissues examined. Similarly, a significant dose-dependent inhibition of the lipid peroxidation caused by DMBA was observed in the BTE-administered animals in all three tissues examined. Our results revealed that BTE provides protection against oxidative damage induced by xenobiotics.
authors.affiliation: Environmental Carcinogenesis Division, Industrial Toxicology Research Centre, Lucknow 226001, India.
authors.forename: Neetu
authors.initials: N
authors.lastname: Kalra
authors.forename: Sahdeo
authors.initials: S
authors.lastname: Prasad
authors.forename: Yogeshwer
authors.initials: Y
authors.lastname: Shukla
mesh_terms: D015127:9,10-Dimethyl-1,2-benzanthracene / Q000037:antagonists & inhibitors; D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D000975:Antioxidants; D028241:Camellia sinensis; D002374:Catalase / Q000378:metabolism; D004793:Enzyme Reactivators / Q000494:pharmacology*; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000201:enzymology; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology; D008297:Male; D051379:Mice; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts / Q000494:pharmacology; D011467:Prostate / Q000187:drug effects / Q000201:enzymology; D013482:Superoxide Dismutase / Q000378:metabolism; D013662:Tea; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D016588:Anticarcinogenic Agents; D000975:Antioxidants; D004793:Enzyme Reactivators; D010936:Plant Extracts; D013662:Tea; D017392:Thiobarbituric Acid Reactive Substances; D015127:9,10-Dimethyl-1,2-benzanthracene; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase