MODULATION OF GLUTATHIONE-S-TRANSFERASE ACTIVITY AND ISOZYME PATTERN IN LIVER AND SMALL-INTESTINE OF RATS FED GOITRIN-SUPPLEMENTED AND T-3-SUPPLEMENTED DIETS

Citation
Mk. Kelley et Lf. Bjeldanes, MODULATION OF GLUTATHIONE-S-TRANSFERASE ACTIVITY AND ISOZYME PATTERN IN LIVER AND SMALL-INTESTINE OF RATS FED GOITRIN-SUPPLEMENTED AND T-3-SUPPLEMENTED DIETS, Food and chemical toxicology, 33(2), 1995, pp. 129-137
Citations number
36
Categorie Soggetti
Toxicology,"Food Science & Tenology
ISSN journal
02786915
Volume
33
Issue
2
Year of publication
1995
Pages
129 - 137
Database
ISI
SICI code
0278-6915(1995)33:2<129:MOGAAI>2.0.ZU;2-3
Abstract
Goitrin is a potent goitrogen that has been shown to induce glutathion e S-transferase (GST) activity and to increase aflatoxin detoxificatio n. In the present study with rats, dietary goitrin (200 mg/kg diet) pr oduced a hypothyroid state and significantly increased levels of hepat ic GSSG (1.4-fold), GST protein (1.4-fold) and GST activity against ch lorodinitrobenzene (CDNB) (1.7-fold). Cotreatment with dietary triiodo thyronine (T-3) reversed these effects in a dose-related manner. Intes tinal GST activities against CDNB and epoxynitrophenoxypropane did not change with goitrin or T-3 treatment. HPLC analyses showed that, in t he liver, goitrin treatment increased the levels of GST-1b and -7 by 3 .5- and 5-fold, respectively, and decreased the level of GST-3 by 50%. Cotreatment with T-3 returned levels of GST-7 and -3 to control level s but only partially reduced the level of GST-1b. In the small intesti ne, goitrin increased the level of GST-1b by 28% and decreased the lev el of GST-7 by 34% compared with those of controls; thyroid hormone tr eatment produced no additional effect on GST in this organ. Selenium d eficiency altered thyroid hormone status but significantly affected th e level only of hepatic GST-3, which was reduced by 30% compared with; that of controls. These results indicate that a modified thyroid hormo nal status plays an important role in the GST-inducing effects of goit rin. A possible mechanism of thyroid-dependent GST induction by goitri n is discussed.