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Antioxidant‐associated chemoprevention by sodium selenite in N ‐nitrosodiethylamine‐induced and phenobarbital‐promoted hepatocarcinogenesis in rats
Author(s) -
Thirunavukkarasu C.,
Babu E.,
Ebrahim A. S.,
Chandramohan N.,
Sakthisekaran D.
Publication year - 2004
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1099
Subject(s) - selenium , antioxidant , phenobarbital , chemistry , pharmacology , medicine , biochemistry , biology , organic chemistry
Abstract The anticarcinogenic/antioxidant potential of sodium selenite (Se), a micronutrient, was evaluated on liver tumourigenesis induced by N ‐nitrosodiethylamine (DEN) and promoted by phenobarbital (PB; 0.05% in diet). Male, albino rats of the Wistar strain were exposed intravenously to a single dose of DEN (200 mg kg −1 body weight). Se (4 ppm in drinking water) was supplemented before initiation, or during initiation and/or during the promotion period of carcinogenesis. At the end of 16 weeks (after DEN administration) nodular incidence, the total number of nodules and non‐enzymic antioxidants such as vitamin E, vitamin C, total thiol, protein thiol and non‐protein thiol contents were measured in hepatoma, surrounding tissue and kidney tissue of control and experimental groups. In hepatoma‐bearing animals the above biochemical changes were decreased when compared with normal control animals. On Se treatment throughout the study, (20 weeks) the above biochemical changes reverted to normal levels. Pre‐ and post‐treatment with Se also shows a tendency to reverse the above changes. The results indicate that prior application of Se significantly reverses the adverse changes produced during the tumourigenesis. Furthermore, prior applications of Se significantly reduced the cumulative number of tumours per tumour‐bearing animals. The present study reveals the antitumour potential of Se against DEN‐induced liver carcinogenesis. Copyright © 2004 John Wiley & Sons, Ltd.