PubMed Health⌕ Search

Biomedical subjects

A Costoff

Publications and source records attributed to A Costoff.

9 recordsLinked to original sources
PubMed1990

Progesterone maintenance of the placental progesterone receptor and placental growth in ovariectomized rats.

These studies examine the trophic effects of progesterone (P) on the progesterone receptor (Rp) and growth of the decidua basalis (DB) and junctional zone (JZ) in the rat placenta. Pregnant rats were ovariectomized (Ovx) in mid-pregnancy and received steroid replacement therapy consisting of implantation of P pellets (25 mg) and injections of estradiol (E), 2 micrograms s.c., daily. Placental protein synthesis, measured by 3H-leucine incorporation in vitro, decreased more than 99% within 24 h of Ovx. However, treatment with P immediately after castration maintained control levels of synthesis. Delay of P treatment for 4 h caused a 60% decline in protein production measured 20 h later (p less than 0.01). Intraperitoneal implantation of a 50-mg pellet of the antiprogestin, RU-38486, in intact pregnant rats decreased protein synthesis by 50% within 6 h and by more than 90% 12 h and 24 h post-implantation (p less than 0.01). Growth of DB and JZ in Ovx rats treated for 48 h with P and/or E was studied both histologically and by changes in protein and DNA content. Rp binding activity was also measured by exchange assay under equilibrium conditions. Only P was able to reverse the effects of Ovx on growth of the DB and JZ. P also maintained Rp levels in the DB above those observed in Ovx and Ovx + E-treated groups (p less than 0.01). The Rp may be a constitutive product in the JZ since binding activity was not altered by Ovx or by steroid treatments. This study shows that P is clearly a trophic hormone of the maternal and chorioallantoic placenta and is essential for placental growth, cellular differentiation, and histological integrity.

Animals↗
PubMed1979

A computer program for the morphometric analysis of cell profiles.

A computer program which yields values for the volumes, surface areas, and volume/surface area ratios of cell profiles is described for use on a desktop calculator (minicomputer). This program uses standard morphometric procedures, and incorporates data obtained from electron micrographs at two levels of sampling. The main program yields values for the 'average cell volume' at the tissue level of sampling. Two options at the cellular level of sampling are also included which yield values for the volumes, surface areas and volume/surface area ratios for the organelles. The first option allows an analysis of 'whole cells' containing equatorial profiles through the nucleus, while the second option permits a 'fractional' approach using segments of the cells. Finally, some of the advantages of the two options are discussed.

Cell Count↗
PubMed1977

Effects of aging on the hypothalamic-hypophyseal-gonadal axis in female rats.

The failure of reproductive function in aged rats could be due to deficiencies at the level of the ovary, pituitary, hypothalamus, or higher brain centers. The classic explanation that the ovary is depleted of follicles does not receive adequate support on the basis of histologic studies of aged ovaries. Basal serum gonadotropin levels change with increasing age in female rats. Serum follicle-stimulating hormone (FSH) levels rise while serum luteinizing hormone (LH) levels fall. Likewise, the characteristic response to castration is markedly altered in aged female rats with a reduced secretion of FSH and a minimal elevation of LH. However, the pituitaires of these animals are still caapable of responding to exogenous LH-releasing hormone with a delayed LH response whose magnitude simulates that seen in younger female animals. With increasing age there is decreased pituitary and/or hypothalamic sensitivity to the feedback action of estradiol. These data are consistent with the postulation that there is an altered hypothalamic-hypophyseal function in aged rats.

Aging↗
PubMed1977

Ultrastructural and physiological studies of the stalk-sectioned rat pituitary gland.

A pituitary stalk-section rat model was prepared that would be suitable for the study of the direct effects of steroids on the pituitary gland. In this model, the hypophyseal stalk was severed surgically and metal foil was inserted to prevent regeneration of portal vessels. The major portion of the pituitary no longer had a direct communication with the hypothalamus, and the only blood supply was from short portal vessels that supply the dorsolateral part of the gland. The effectiveness of the lesion was demonstrated by very high levels of serum prolactin and very low FSH and LH. Light microscopic examination revealed a large infarct in the central region of the gland with stainable cells in the peripheral area. Fourteen days after stalk-section, the infarct had shrunken appreciably, and after 21 days it was replaced by a scar. Ultrastructural studies revealed the presence of functional mammotropes in the peripheral regions of the pituitary gland, while other cells were smaller, less active, and contained fewer secretory granules. After LHRH administration there was an increase in serum LH, thus indicating the presence of a substantial number of viable gonadotropes. This was confirmed by the ultrastructural findings which now showed the appearance of large, well-granulated gonadotropes. When LHRH was given to estradiol 17-beta primed ovariectomized stalk-sectioned rats, there was a great augmentation of LH release, and many castration cells were now apparent. Therefore, the administration of estrogen and LHRH was needed for the gonadotropes of the isolated pituitary to function optimally in the synthesis and secretion of FSH and LH. The stalk-sectioned animal model permits evaluation of pituitary function isolated from hypothalamic control while it leaves the surviving pituitary gland in its normal anatomical position.

Animals↗
PubMed1976

Actions of pregnant mare serum gonadotropin in the immature female rat: correlative changes in blood steroids, gonadotropins, and cytoplasmic estradiol receptors of the anterior pituitary and hypothalamus.

Several blood steroids, serum gonadotropins and cytosol estradiol receptors of the anterior pituitary and hypothalamus were quantified in immature female rats which were induced to ovulate with pregnant mare's serum gonadotropin (PMSG). Studies revealed that serum levels of progesterone, 17-hydroxyprogesterone, testosterone, androstenedione and estradiol were initially elevated at 6 PM (day 30) after administration of 8 IU of PMSG at 10 AM day 30. Serum levels of estradiol and testosterone rose progressively from day 30 through the AM of day 32. A further increase in serum concentrations of progesterone, 17-hydroxyprogesterone, androstenedione, testosterone, and dehydroepiandrosterone occurred on the PM of day 32 whereas serum estradiol levels declined. Serum levels of all steroids declined on the day of estrus (33) and only progesterone levels were further elevated on day 34 (diestrus). Dihydrotestosterone concentrations were minimally altered by PMSG treatment. Saline administration resulted in no significant alterations in levels of any steroid quantified from day 29 to 34 in control animals. A progressive decline in cytosol estradiol receptor content of the anterior pituitary and hypothalamus was documented following PMSG treatment of intact female rats; there was no depletion of receptors following PMSG administration to ovariectomized immature rats. Maximal depletion of cytosol estradiol receptors occurred on day 32 with replenishment of cytosol estradiol receptor levels on estrus (day 33). The preovulatory gonadotropin surge was found to occur on the PM of day 32 after maximal receptor depletion. The cycle of depletion and replenishment of receptors was repeated during a second spontaneous estrous cycle four days later which coincided with a rise and fall in serum estradiol levels. It is suggested that the depletion of cytosol estradiol receptors of the anterior pituitary/hypothalamic unit may be causally related to the preovulatory gonadotropin surge resulting from PMSG administration to immature female rats. In addition, changes in blood steroids and gonadotropins after PMSG treatment are similar to those reported for proestrus-estrus-diestrus I of the normal adult estrous cycle. These findings further demonstrate the validity of the PMSG-primed immature female rat preparation as a model for the estrous cycle of the adult rat.

Androstenedione↗
PubMed1975

Primordial follicles with normal oocytes in the ovaries of postmenopausal women.

In ultrastructural studies, the ovaries of postmenopausal women were compared with those of pre- and perimenopausal women. Primordial follicles containing apparently normal oocytes were found in all postmenopausal ovary samples. Differentiating follicles were often found in these samples, but they were in various states of atresia. The findings suggest that the menopause does not result exclusively from exhausation of the primordial follicles.

Adult↗
PubMed1975

Influence of estrogen-progesterone combinations on gonadotropin secretion in castrate female rats(1).

In order to study the effect of progesterone in modulating the secretion of gonadotropins, various doses of progesterone were administered to castrated immature and mature female rats. Progesterone did not prevent the postcastration rise of FSH and LH in these animals. Various amounts of progesterone were then administered to castrated rats that were treated with a constant low dose of estradiol. In animals given doses of estradiol that were able to decrease serum FSH and LH below castrate levels, but not to prevent the post-castration rise, the effect of progesterone was dose-dependent. A very low dose of progesterone lowered serum gonadotropins, an intermediate dose brought about an increase in secretion, and high doses were suppressive. The modifying action of progesterone appears to be dependent upon the level of estrogen, the dose of progesterone, and the time of administration.

Age Factors↗
PubMed1975

Dehydroepiandrosterone-induced polycystic ovaries and acyclicity in the rat.

Administration of dehydroepiandrosterone (DHA) to the immature female rat resulted in one precocious ovulation followed by ovulatory failure. The animals exhibited either "constant-estrus" or "constant-diestrus" vaginal smears, and the ovaries were either polycystic or contained corpus luteum-like structures. Serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels showed an ovulatory type surge on day 30, at the time of the precocious ovulation. Thereafter, serum FSH levels were comparable to those of control rats, whereas the LH levels were very low. Serum prolactin was elevated significantly in DHA-treated animals. The ovaries of DHA-treated animals were responsive to gonadotropins and the pituitary was responsive to luteinizing hormone-releasing hormone. Withdrawal of androgen treatment resulted in restoration of cyclicity. This animal model demonstrates that an androgen insult can cause ovulatory failure and polycystic ovaries in spite of normal ovaries, adrenals, and hypothalamic-pituitary mechanisms. That such ovulatory failure is a result of the androgen administration is further substantiated by restoration of cyclicity after androgen withdrawal. This animal model in several ways is similar to the human polycystic ovary syndrome and has a potential application in the study of the mechanism of androgen-induced ovulatory failure.

Animals↗