BIOCHEMICAL BASIS OF SELENOMETHIONINE-MEDIATED INHIBITION DURING 2-ACETYLAMINO-FLUORENE-INDUCED HEPATOCARCINOGENESIS IN THE RAT

Citation
B. Mukherjee et al., BIOCHEMICAL BASIS OF SELENOMETHIONINE-MEDIATED INHIBITION DURING 2-ACETYLAMINO-FLUORENE-INDUCED HEPATOCARCINOGENESIS IN THE RAT, European journal of cancer prevention, 5(6), 1996, pp. 455-463
Citations number
43
Categorie Soggetti
Oncology
ISSN journal
09598278
Volume
5
Issue
6
Year of publication
1996
Pages
455 - 463
Database
ISI
SICI code
0959-8278(1996)5:6<455:BBOSID>2.0.ZU;2-X
Abstract
Supplementation of selenium in the form of selenomethionine (8 ppm) in drinking water daily has been found to be highly effective in reducin g cancer incidence in male Sprague-Dawley rats fed 2-acetylamino-fluor ine (2-AAF) (0.05%) in the basal diet daily for 16 weeks, Selenomethio nine treatment before initiation, during initiation or during the sele ction/promotion phases of hepatocarcinogenesis has been found to be ef fective in elevating hepatic microsomal cytochrome b5, cytochrome P-45 0 contents, triphosphopyridine nucleotide-cytochrome c-reductase and c ytosolic aryl hydrocarbon hydroxylase activities to a statistically si gnificant level measured either in the hyperplastic nodules or in the non-nodular surrounding liver parenchyma compared with 2-AAF control r ats, Moreover, selenomethionine treatment throughout the study also de creased the cytosolic 1-chloro-2,4-dinitrobenzene conjugated glutathio ne-S-transferase and microsomal UDP-glucuronyl transferase activities to a significant level when compared with 2-AAF control rats, Furtherm ore, direct correlations between hyperplastic nodules and non-nodular liver areas were observed with the hepatic selenium content and also w ith the rates and patterns of hepatic drug metabolism, Selenomethionin e was also found to protect and improve the histopathological indices without any toxic side effects as revealed from the haematoxylin and e osin staining. Our results establish the fact that selenium is particu larly protective in limiting the action of 2-AAF during the initiation phase of hepatocarcinogenesis.