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Lectins, calcium ionophore A23187 and peanut oil as deciduogenic agents in the uterus of pseudopregnant mice: effects of tranylcypromine, indomethacin, iproniazid and propranolol.

Intraluminal injections of lectins, including concanavalin A (Con A), wheatgerm lectin, and soybean lectin, Con A-Sepharose 4B beads, calcium ionophore A23187 or peanut oil into the left uterine horns of mice on day 4 of pseudopregnancy induced the formation of deciduomata and significantly increased the weight and alkaline phosphatase activity of uterine tissue on day 7 of pseudopregnancy. In contrast, injections of these materials into the uterine horns of non-pseudopregnant mice that had not been previously mated failed to induce similar responses. Tranylcypromine blocked the decidual cell reaction artificially induced by lectins, calcium ionophore A23187 and peanut oil in pseudopregnant mice. However, uterine responses observed after individual and concurrent injections with indomethacin, iproniazid, propranolol or progesterone indicated that this deciduoma-blocking effect may not be solely related to the ability of tranylcypromine to inhibit prostacyclin biosynthesis but may also involve catecholamines and luteolytic prostaglandins which interfere with decidualization on day 4 and day 6 of pseudopregnancy, respectively. A role for prostaglandins and uterine beta-adrenergic receptors, however, was implicated in the induction of decidualization because both indomethacin and propranolol blocked the response to peanut oil. The results suggested that the embryonic signal responsible for the induction of the decidual cell reaction in mice may involve surface interactions between the embryo and uterine luminal epithelium resulting in a stimulation of the uterus via glycoprotein receptors. A role for calcium was implicated in this phenomenon.

Animals↗

Antibody-recognized [125I]estradiol-receptor complex in ovarian epithelial carcinoma.

Monoclonal antibody against human breast cancer estrogen receptor was used to demonstrate binding of a gamma- and Auger electron-emitting estrogen to the estrogen receptor in ovarian epithelial carcinomas. When cytosols of estrogen receptor-rich ovarian adenocarcinomas were analyzed on sucrose gradients containing 0.4 M KCl, the presence of monoclonal antibody against breast cancer estrogen receptor caused a binding peak for [125I]- and [3H]estradiol to shift from the 4S to the 8-9S region, indicating antibody complex formation with ovarian adenocarcinoma estrogen receptor. The antibody-shifted peak of 8-9S [125I]- and [3H]estradiol binding was totally inhibited by a 100-fold molar excess of diethylstilbestrol (DES), but not by testosterone or progesterone, indicating a preference for estrogen binding by the antibody-shifted estrogen receptor. When estrogen receptor from the nuclear fraction of ovarian adenocarcinomas was incubated with [125I]estradiol at 1C, in the presence of 0.4 M NaSCN to facilitate exchange with endogenous ligand, binding occurred that was inhibitable by DES and restricted to the 4S region. Under these conditions the nuclear estrogen receptor was also shifted to the 8-9S region by the presence of the monoclonal antibody against estrogen receptor.

Adenocarcinoma↗

Control of luteal function in the mink (Mustela vison).

The ranch mink was studied to determine the role of pituitary luteotrophins on corpus luteum (CL) function before and after implantation. Twelve mink were treated with monoclonal antiserum against gonadotrophin-releasing hormone (GnRH), and 12 with an irrelevant monoclonal antibody during embryonic diapause. Activation of the CL, plasma progesterone concentration and embryo implantation were unaffected by this treatment. In a second trial, groups of ten mink were treated with GnRH antibodies, bromocriptine, bromocriptine plus 0.5 mg prolactin per day per animal, or ethanol vehicle. Comparison of the consequent profiles of progesterone indicated that both bromocriptine and anti-GnRH compromised postimplantation CL function by inducing regression of the corpus luteum. Incubation of dissociated luteal cells from ovaries of mink at 21-24 days after implantation with either LH or prolactin increased the accumulation of progesterone over 2 h. Addition of 25-hydroxy-cholesterol (25OHC) as substrate increased basal levels and the progesterone accumulation stimulated by LH and prolactin; the increases induced by luteotrophins were additive. There was an apparent synergistic interaction between prolactin and canine low-density lipoproteins (LDL) in the stimulation of progesterone secretion in vitro. The results are interpreted to indicate that LH/FSH are not required for luteal support during embryonic diapause, or for luteal activation. Prolactin is necessary for luteal activation, and LH and/or FSH and prolactin are obligate luteotrophins during the postimplantation period in the mink.

Animals↗