title: Modulation of glutathione S-transferase activity and isozyme pattern in liver and small intestine of rats fed goitrin- and T3-supplemented diets.
abstract: Goitrin is a potent goitrogen that has been shown to induce glutathione S-transferase (GST) activity and to increase aflatoxin detoxification. In the present study with rats, dietary goitrin (200 mg/kg diet) produced a hypothyroid state and significantly increased levels of hepatic GSSG (1.4-fold), GST protein (1.4-fold) and GST activity against chlorodinitrobenzene (CDNB) (1.7-fold). Cotreatment with dietary triiodothyronine (T3) reversed these effects in a dose-related manner. Intestinal GST activities against CDNB and epoxynitrophenoxypropane did not change with goitrin or T3 treatment. HPLC analysis showed that, in the 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 T3 returned levels of GST-7 and -3 to control levels but only partially reduced the level of GST-1b. In the small intestine, goitrin increased the level of GST-1b by 28% and decreased the level of GST-7 by 34% compared with those of controls; thyroid hormone treatment produced no additional effect on GST in this organ. Selenium deficiency altered thyroid hormone status but significantly affected the level only of hepatic GST-3, which was reduced by 30% compared with that of controls. These results indicate that a modified thyroid hormonal status plays an important role in the GST-inducing effects of goitrin. A possible mechanism of thyroid-dependent GST induction by goitrin is discussed.
authors.affiliation: Department of Nutritional Sciences, University of California, Berkeley 94720.
authors.forename: M K
authors.initials: MK
authors.lastname: Kelley
authors.forename: L F
authors.initials: LF
authors.lastname: Bjeldanes
mesh_terms: D000818:Animals; D013956:Antithyroid Agents / Q000494:pharmacology*; D002851:Chromatography, High Pressure Liquid; D004137:Dinitrochlorobenzene / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004790:Enzyme Induction / Q000187:drug effects; D005527:Food, Fortified; D005978:Glutathione / Q000031:analogs & derivatives / Q000378:metabolism; D019803:Glutathione Disulfide; D005982:Glutathione Transferase / Q000096:biosynthesis / Q000378:metabolism*; D007421:Intestine, Small / Q000187:drug effects* / Q000201:enzymology; D007527:Isoenzymes / Q000096:biosynthesis / Q000378:metabolism; D008099:Liver / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D010080:Oxazoles / Q000008:administration & dosage / Q000494:pharmacology*; D023303:Oxazolidinones; D051381:Rats; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000172:deficiency; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D013956:Antithyroid Agents; D004137:Dinitrochlorobenzene; D007527:Isoenzymes; D010080:Oxazoles; D023303:Oxazolidinones; D014284:Triiodothyronine; C004333:goitrin; D013972:Thyrotropin; D005982:Glutathione Transferase; D005978:Glutathione; D012643:Selenium; D013974:Thyroxine; D019803:Glutathione Disulfide