413 Genital cycle modifications during afp hepatocarcinogenesis in female rat

413 Genital cycle modifications during afp hepatocarcinogenesis in female rat

413 GENITAL CYCLE MODIFICATIONS DURING AFP HEPATOCARCINOGENESISIN FEMALE RAT. SERALINI G-E., CASTELLI D., DONZEAU M., LAFAURIE M., KREBS B. et STOHA ...

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GENITAL CYCLE MODIFICATIONS DURING AFP HEPATOCARCINOGENESISIN FEMALE RAT. SERALINI G-E., CASTELLI D., DONZEAU M., LAFAURIE M., KREBS B. et STOHA C. Fat, i&d.,U 210 lNSEX@l,Lab. Immmolcgie, CheminVallcmh-ose, 06034 Nice, France. During chemical hepatocarcinogenesisthe endocrine glands show important modifications in both sexes of the rat. In female, a marked ovarian atrophy leads to a decrease of folliculsr maturation, an early fall of theplasmaprogesterone level, while estrogen values remain normal. The study of the genital cycle in the rat during hepatocarcinogenesisby acetylaminofluorene (AAF), confirms these results with clear irregularity after 50 days of carcinogenic diet and entire blockade of genital cycle in metestrus after 70 days. A role of alpha-fetoprotein,which is reexpressed during liver carcinogenesisby AAF, is suggested for the regulation of ovarian activity.

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DISTRIBUTION OF ANDROGRN AND ESTROGEN RECEPTORS AMONG HUMAN PERIPHERAL T LYMPHOCYTE SUBSETS. L.DANELt J.H.M.COHRNfCG.CORDIERj+J.P.RRVILLbR@+ S.SAEZ+ Centre L&on Bgrard+, U SO HSpital Edouard Herriotj+69008 LYON, FRANCE The immune response has been reported to be modulated by sex hormones in several models and estrogen receptorshave been demonstrated in human thymus. We therefore investigated the presence of estrogen and androgen receptors among peripheral T cells. Thoracic duct lymph provided large amounts of circulating lymphocytes. Pure T cells were obtained by negative selection using complement - dependent cytotoxicity with a monoclonal antibody against a monomorphic determinant of class If histocompatibility antigen (HLA DRf. Futhermore subsets of 0KT8 positive and OKTS negative lymphocytes were selected using an OKT8-like monoclonal antibody. Sex steroid binding was determined on purified3nuclei. No androgen receptors could be found on peripheral T cells. The cytoplasmic ( H) 178 -estradiol-receptorcomplex was always translocated to the nucleus in vitro in one hour at 37'C. No estrogen receptors were demonstrable on purified 0KT4 positive subsets. Assuming that estrogen receptors were evenly distributed among OKTS positive cells, their level could be estimated to be about 40 fmol/mg DNA. The restriction of estrogen receptors to T cells bearing the "suppressor-cytotoxic" phenotype suggests a possible pathway for the modulation of T cell suppressive activities by estrogens.

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OF SOlXE S!i!EROID HOB.MOTiEs 01J THZ HEItiOl?OIETI(: S'JXM CZLL ACTIVI'I'Y V.A.Ko~;~I&;e~rlova . ..a

stem cells,defined'here as spleen colony-forming units CFU-S,in the marrow of a no~al,healthy mouse are proliferatively quiescent,The results of our investigation indicate that steroid hormones can either trigger the entr of &Q-S into DEA-synthesis in the case of testosterone-propionate(TSP 4 or inhibit,ths proliferative activity of CFU-S in the case of hydrooortysone(iiC).GFU-S migration correlates strictly with their proliferative activity.TSP-induced stimulation of marrow stem cell proliferative activity has been shown to be accomponied by a high entry of the latter in the blood circulation in the S-phase,Obviou8ly,~SP also reduce8 the duration of the eel_1cycle by foure hours,that was revealed by Vassort's methsd(Vassort et al. ,1973).The reduction in cell cycle duration was the cause of primary stem cell differentiation in erythropoiesis and reduction of B-cell production.Thus steroid hormones influence upon the proliferative status of the CPU-S that leads to some interdependent alterations of migrative and differentiative processes,the role of which is discussed.

Haemopoietic