title: Dietary influence of selenium on the incidence of N-nitrosodiethylamine-induced hepatoma with reference to drug and glutathione metabolizing enzymes.
abstract: 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, gamma-glutamyl transpeptidase, gamma-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.
authors.affiliation: Department of Medical Biochemistry, Dr ALM PG Institute of Basic Medical Sciences, University of Madras, Chennai-600 113, India.
authors.forename: C
authors.initials: C
authors.lastname: Thirunavukkarasu
authors.forename: J
authors.initials: J
authors.lastname: Prince Vijeya Singh
authors.forename: M
authors.initials: M
authors.lastname: Thangavel
authors.forename: K
authors.initials: K
authors.lastname: Selvendiran
authors.forename: D
authors.initials: D
authors.lastname: Sakthisekaran
mesh_terms: D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology*; D001189:Aryl Hydrocarbon Hydroxylases / Q000378:metabolism; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced* / Q000378:metabolism; D015786:Cytochromes b5 / Q000378:metabolism; D003600:Cytosol / Q000201:enzymology; D004052:Diethylnitrosamine / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008862:Microsomes, Liver / Q000378:metabolism; D009251:NADPH-Ferrihemoprotein Reductase / Q000378:metabolism; D009374:Neoplasms, Experimental / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D012643:Selenium / Q000494:pharmacology*
chemical_list: D016588:Anticarcinogenic Agents; D000975:Antioxidants; D004052:Diethylnitrosamine; D015786:Cytochromes b5; D001189:Aryl Hydrocarbon Hydroxylases; D009251:NADPH-Ferrihemoprotein Reductase; D005982:Glutathione Transferase; D005978:Glutathione; D012643:Selenium