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Dietary influence of selenium on the incidence of N‐nitrosodiethylamine‐induced hepatoma with reference to drug and glutathione metabolizing enzymes
Author(s) -
Thirunavukkarasu C.,
Prince Vijeya Singh J.,
Thangavel M.,
Selvendiran K.,
Sakthisekaran D.
Publication year - 2002
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.979
Subject(s) - selenium , glutathione , chemistry , phenobarbital , microsome , reductase , glutathione reductase , selenium deficiency , biochemistry , enzyme , cytochrome p450 , cytosol , medicine , endocrinology , pharmacology , biology , glutathione peroxidase , organic chemistry
The dietary administration of selenium (sodium selenite; 4 p.p.m.) daily has been found to be highly effective in reducing the incidence of cancer induced by N‐nitrosodiethylamine (DEN) in Wistar strain rats. Selenium treatment either before initiation, during initiation and selection/phenobarbital promotion phases of hepatocarcinogenesis has been found to be effective in elevating hepatic microsomal cytochrome b 5 , NADPH‐cytochrome C reductase and cytosolic aryl hydrocarbon hydroxylase activities to a statistically significant level measured either in the hyperplastic nodule or in the surrounding liver tissues compared to control animals. Moreover, selenium treatment throughout the study, decreases the cytosolic glutathione S‐transferase and microsomal UDP‐glucuronyl transferase activities by a significant degree when compared to control rats. Alterations in glutathione metabolizing enzyme activities (glutathione reductase, γ‐glutamyl transpeptidase, γ‐glutamylcysteine synthetase and glucose‐6‐phosphate dehydrogenase) were also observed in selenium‐treated groups. Our results confirm the fact that selenium is particularly protective in limiting the action of DEN during the initiation phase of hepatocarcinogenesis. Copyright © 2002 John Wiley & Sons, Ltd.