Hypophyseal regulation of hepatic histidase during postnatal development and adulthood: II. Pituitary-estrogen interrelationship

Estrogen, which augments rat liver histidase activity in pre- and postpubertal rats, is ineffective in hypophysectomized animals, in which enzyme activities are already elevated. This failure of estrogen action has been demonstrated in hypophysectomized weanling, as well as adult females, the former of which manifest enzyme activities considerably below maximum possible values. The following agents, which are known to suppress histadase activity under certain conditions, were ineffective in permitting estrogen stimulation of histadase in hypophysectomized rats: glucocorticoid, testosterone, adrenocorticotrophin acting extra-adrenally and via the adrenals, growth, and preparations of whole pituitaries of bovine or female rat origin. The following materials, which do not themselves alter enzymic activity, were likewise incapable of permitting estrogenic enhancement of histadase activity in these animals: follicle-stimulating hormone and luteinizing hormone acting extra-gonadally, thyrotrophic hormone, and bovine posterior pituitary preparations.     

Endocrine control of spermatogenesis in primates

Control of primate spermatogenesis is reviewed in terms of endogenous regulatory mechanisms and endocrine approaches to contraception and treatment of infertility. The role of gonadotropins and steroid hormones in maintaining spermatogenesis in primates is incompletely understood because A) hormonal interactions are complex, and B) most studies have used rodents rather than primates. Feedback control, interaction of LH and testosterone, the role of androgen, androgen in secondary sex organs, regulation of receptor proteins, roles of prolactin and growth hormone, and the breakdown and modification of the endocrine control mechanism are reviewed. The treatment of infertility with GnRH, gonadotropins, and androgen is discussed. Information is included on contraception research using the following methods: immunization against GnRH, use of GnRH analogs, immunization against gonadotropins, induced suppression of FSH secretion or action, and steroid suppression of spermatogenesis. The importance of studying testicular steroid metabolism in primates is stressed. Significant advances in the understanding of endocrine control of spermatogenesis have been made in recent years, but no primate species have been thoroughly studied. Variability between species in endocrine control mechanisms is an important factor in selecting primate models, and it is clear that such models can be valuable in the development of male contraceptives.     

Anti-human gonadotropin antibodies generated during in vitro fertilization (IVF)-related cycles: Effect on fertility of rhesus macaques

Administration of human gonadotropins such as hFSH, hLH, and hCG to rhesus macaques can result in formation of anti-human gonadotropin antibodies. To determine whether the presence of these antibodies interferes with subsequent fertility, sixteen female rhesus macaques (Macaca mulatta) with known antibody levels were bred with male rhesus macaques. The presence of antibodies did not interfere with conception or maintenance of pregnancy. Furthermore, antibody titers did not increase during gestation or following the resolution of pregnancy.     

Effect of follicle-stimulating hormone on metabolism and maturation in Bufo arenarum oocytes

In the fully grown Bufo arenarum oocyte, carbohydrate breakdown during the autumn-winter season is accomplished mainly through the glycolytic pathway followed by the krebs cycle. During the breeding season (spring-summer), carbohydrates are used mainly through the pentose phosphate cycle and through the variant of the Krebs cycle known as the glutamic aspartic cycle. The metabolism operating in the oocytes was determined using the following paramenters: 1) the capacity of isolated mitochondria to oxidize citrate and fumarate; 2) the enzymatic activities of phosphofructokinase (PEK) and glucose-6-phosphate dehydrogenase (G-6-PDH); and 3) cirate and ATP compartmentalization. The present paper shows that follicle-stimulating hormone (FSH) would be one of the factors responsible for summer metabolism, since ovary fractios obtained from winter specimens treated with the hormone acquired the metabolic characteristics corresponding to oocytes obtained from breeding-season animals from dose-response, and response in the function of time curves, it could be assumed that the optimum doses and times were 0.1 μg FSH/ml of incubation medium and 30 min treatment, respecitively. The metabolic effect of FSH upon oocytes could be mediaated by the adenylate cyclase cAMP system, since treatment of ovric fractions with cAMP 10-³ M reproduced the effects obtained with the hormone. In addition, 0.02 mg/ml tetracyline proved to block the effect of FSH. A direct metabolic action of FSH on body cavity oocytes (without follicle cells) was observed when submitting these oocytes to the same hormonal treatment.