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Journal of Environmental Pathology, Toxicology and Oncology
Impact-faktor: 1.625 5-jähriger Impact-Faktor: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

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

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v26.i1.20
pages 9-20

Abrogation of Thioacetamide-Induced Biochemical Events of Hepatic Tumor Promotion Stage by Tannic Acid in Wistar Rats

Anuradha Sehrawat
Section of Chemoprevention and Nutrition Toxicology, Department of Medical Elementology and Toxicology, Faculty of Science, Jamia Hamdard (Hamdard University), New Delhi 110 062, India
Sarwat Sultana
Section of Molecular Carcinogenesis and Chemoprevention, Department of Medical Elementology and Toxicology, School of Chemical and Life Sciences amia Hamdard, New Delhi, India


Tannic acid is present in almost every edible plant and is generally used as a safe food additive. In this study we investigated the antioxidative and antihyperproliferative potential of tannic acid against thioacetoamide (TAA), a potent hepatotoxic-substance-induced oxidative stress and hyperproliferation biomarker. We have shown here that the activities of hepatic antioxidant enzymes, phase II metabolizing enzymes, and the glutathione content were decreased while hepatic ornithine decarboxylase activity and DNA synthesis were induced in TAA-treated animals. Tannic acid administration at two different doses prior to the TAA injection partially recovered the depleted level of glutathione, inhibited activities of antioxidant and phase II metabolizing enzymes, and resulted in significant inhibition of oxidative stress in a dose-dependent manner. Tannic acid administration before TAA treatment also resulted in a significant decrease in ODC activity and [3H]-thymidine incorporation in rat liver, which are classical markers of inflammation and tumor promotion. Our data clearly demonstrate that tannic acid possesses antioxidant and antiproliferating activities because it inhibits early biomarkers of TAA-induced tumor promotion in an in vivo animal model.

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