title: Effect of chronic thyroxine treatment on pregnancy in rats: effects on oestrogen, progesterone, prolactin and GH receptors in uterus, liver and mammary gland.
abstract: We have previously shown that experimental hyperthyroidism produces premature and difficult delivery and absence of lactation in spite of apparently adequate luteolysis and lactogenesis. To study the possible causes of these alterations we measured the effect of treatment with T4 (0.25 or 1 mg kg(-1), s.c., daily, started 10-15 days before mating, HT0.25 and HT1) on serum hormones and their receptor (R) concentrations in reproductive tissues on day 20 of pregnancy (1800 hours), comparing them with controls on the same day (C20), or on day 21 of pregnancy (1800 hours) (C21). Serum prolactin (PRL) and corticosterone (B) concentrations increased in the HT groups, progesterone (Pg) and GH decreased and estradiol (E2) did not change, compared with C20 group. C21 rats had increased serum PRL and decreased Pg and GH. In HT rats mammary DNA and protein tissue content was doubled. Receptor concentrations were expressed per mg DNA. Mammary PRL-R were increased in HT1 rats, while E-R and Pg-R were significantly lower in both HT groups. HT0.25 and HT1 rats had increased uterine E-R and Pg-R and decreased liver PRL-R and GH-R as well as their mRNAs. Liver E-R, PRL-R and GH-R were decreased in C21 rats, while uterine Pg-R were increased. Thus, some of the observed changes (serum Pg and GH, mammary and uterine Pg-R, and liver GH-R and PRL-R decreases and serum PRL increase) may be due at least partially to the advancement in luteolysis and delivery, being similar to the changes observed between days 20 and 21. The changes in serum B, mammary PRL-R, and mammary and uterine E-R may be caused solely by the T4 treatments and may play a role in the alterations previously observed.
authors.affiliation: Laboratorio de Reproducción y Lactancia, CRICYT-CONICET, Mendoza, Argentina.
authors.forename: R R
authors.initials: RR
authors.lastname: Rosato
authors.forename: H
authors.initials: H
authors.lastname: Jammes
authors.forename: G A
authors.initials: GA
authors.lastname: Jahn
mesh_terms: D000818:Animals; D003345:Corticosterone / Q000097:blood; D003600:Cytosol / Q000378:metabolism; D004247:DNA / Q000032:analysis; D004958:Estradiol / Q000097:blood; D005260:Female; D013006:Growth Hormone / Q000097:blood; D006728:Hormones / Q000097:blood*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008321:Mammary Glands, Animal / Q000187:drug effects* / Q000378:metabolism; D008565:Membrane Proteins / Q000032:analysis; D011247:Pregnancy; D011374:Progesterone / Q000097:blood; D011388:Prolactin / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface / Q000378:metabolism*; D011959:Receptors, Estradiol / Q000378:metabolism; D018013:Receptors, Neuropeptide / Q000235:genetics / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D013974:Thyroxine / Q000494:pharmacology*; D014599:Uterus / Q000187:drug effects* / Q000378:metabolism
chemical_list: D006728:Hormones; D008565:Membrane Proteins; D011956:Receptors, Cell Surface; D011959:Receptors, Estradiol; D018013:Receptors, Neuropeptide; D011980:Receptors, Progesterone; D011374:Progesterone; D004958:Estradiol; D011388:Prolactin; D013006:Growth Hormone; D004247:DNA; D013974:Thyroxine; D003345:Corticosterone