Document KRVXo7akJx6RK0v54YbD4qBGo

uriabaorbed etMoninefvaV''"later excreted In the feces. Dur Ing the passage through the gastrointestinal tract, a . portion of.methionine was metabolized. The face of absorbediieUhionine was investigated In the small intestine, Oliver, blood, kidney, and urine as a function of time after application. A great part of ethionine was quickly oxidized to ethionine sul foxide.. In liver and kidney, the concentration of ethionine sulfoxide was higher than that of free ethionine. In all organs, the presence of N-acctylethionine sulfoxide was alsotdemonstrated. Ethio nine sulfoxide can be reduced,Land fY-acetylethionine can be deacetylated in vivo as demonstrated by the formation of S-adenosylethionine from ethionine sulfoxide and //-acetylethionine. In urine, four M *. 1 . *>L J _ Carcinogenesis Abstracts Vol. 13, No. 7 July, 1975 , oooo; MUTAGENICITY W VITRO AND POTENTIAL CAR- ------ CINOGENICITY OF CHLORINATED ETHYLENES AS A.FUNCTION OF METABOLIC OXIRANE FORMATION. (Eng.) (Creim, H. .(Dept. Toxicology of Gesellschaft fur S trahlenund'Uruweltforschung, 8042 Munchen-Neuher- berg, West Germany); Bonse, G.; Radwan, Z.; Reich ert, D.; Henschler, D. Biochem. Pharmacol. 24(21); 2013-2017; 1975. The mutagenicity of six chlorinated ethylenes formed during microsomal activation was.tested in a meta bolizing ipiyitro system with Eaoherichia coli K\2 Mutation rates were//determined . for three back muta tion systems gal-f-, arg+t and nad+,,and for the MTR system where forward mutation leads to resistance to 5-methyl-rDL-tryptophan. Cells were Incubated CARCINOGENESIS ABSTRACTS VOL. XIII lene.` thiourea/TO 5, 25, 125, 250| the weighta of dal uptake of \|jj the criteria stt carcinogen for t levels and a th> It caused a slig 25 ppm feeding <1 noticeably rever that were change ETU diets. ETtlJ was not biologic; data support the: plasia in the ra/ macological st of excessive.;ehd; se of the rj /fthvone^eel. ^DIFFER ;SOCIATION^'WlJ AND PERPHENAZINE (Div. Diabetes a: and Res. Foundat Salocks, C. B.;1 97 (5):1112-1122; V, i Prolactin (PUL)/i in strains of mic mary tumors and,,;t were compared. pituitary and sei erally higher in| mammary tumors. had little correll mary tumors in di^j concentrations ir ip) followed the the strain: C3H/f -I'"' uM JULY 1975 iw; y-w1,- * 'f' "kY , v-. ? v. :?V'-, , ../.>f4. . . ^ . - -'-1K.mv'rt/fe.r./' : r-fr-'z ^ , (3687-3690) /0(0'2521 1-15W for two nobra with microsomal protein from mouse liver, an NADPH-generating system with 5 pM MgCl2. and various concentrations of the test compounds: tetrachloroethyleneffitrichloroethylene (TRI&11,1- Jichloroethylene (1,1-DCE) ^cis-l ,2-dichloroethylene, ran8-1,2-dichloroethylene, an&vinyl chloride (VCM77 Only those compounds (VCM, 1,1-DCE, and TRI) that form very unstable oxiranes induced mutations in the test system. The highest mutation rates were detected in the arg+ system; the other systems were less sensitive to the mutagenic effects of the meta bolites. .The mutagenicity of TRI was unexpected, and further study of the mutagenic and potentially carcinogenic properties of this compound are recom mended . Carcinogenesis Abstracts Vol. 13, No. 7j July, 1975 Five groups of 68 male and 68 female Charles River rats, approximately five weeks old, were fed ethy lene thiourea (ETU) for two years at levels of 0, 5, 25, 125, 250 or 500 ppm in the diet. . Body weights, the weights of the thyroid and other organs, thyroi dal uptake of 131 I, hematology, and histology were the criteria studied. ETU was found to be a thyroid carcinogen for the rat at the,.250 and 500 ppm dietary levels and a thyroid tumorigen at the 125 ppm level; it caused a slight thyroid hyperplasia at the 5 and 25 ppm feeding levels. Thyroid hyperplasia was not noticeably reversible in those rats in each group that were changed to control diet after 66 wk on ETU diets. ETU ingestion at the 5 and 25 ppm levels was not biologically deleterious to the rat. The data support the view that ETU-induced thyroid neo plasia in the rat ,are the result of excessive phar macological stimulation, i.e.," they occur because of excessive endocrine organ stimulation and not because of the reaction of one molecule of carcino gen with one cell|to initiate neoplasia; dence strains, had 200 ng/ml; C57BL/J incidence strains'^ the medlum-inclden level. The rateLo with high inciden than in those wit had no inf luence'o The strain-specif centrations were Ileal and diurnal^, levels were gener phase and lower estrous cycle in b It is possible tha may be an imports "ors. o / yyjTRo w oo ;&Kl8t 55(l):`35-36; 1975; . .1c The growth effect human prolactin o tissue from 30 wo used at 5 yg/ml. chlcine (0.1 pgA to each culture, were counted in epithelium surviv little mitosis orf hormones in vitxwi activity of cultu of human prolactin tivity over that o addition of ovine? crease in the Ins results 8uggest'?t* breast tissue can. further studlesTto of prolactin in vi man prolactin