Plasma Follicle-stimulating Hormone Concentrations Research Articles

Effects of induction of parturition by administration of a prostaglandin F 2α analogue in rabbits: possible modification of prolactin, LH and FSH secretion patterns

The influence of inducing parturition by the administration of prostaglandin F 2α (PGF 2α) on prolactin (PRL), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion patterns during the last days of pregnancy (Days 29–31) and lactation (Days 1–28) was studied in 20 doe rabbits of the California breed. Animals were allocated to receive either a single intramuscular injection of 50 μg of a PGF 2α, analogue (treated group) or 2 ml saline (control group) on Day 29 of pregnancy. All females were mated on Day 7 post-partum. The conception rate in treated and control animals was 100% and 90%, respectively. No influence of the prostaglandin treatment on mean plasma PRL and FSH concentrations was observed. High plasma PRL levels were detected in both groups from Day 7 to 19 of lactation. PRL levels decreased in all rabbits from Day 19 to 28 of lactation. Prostaglandin F 2α-treatcd animals showed low plasma LH concentrations after treatment during the entire period studied. High mean FSH concentrations were found in both groups from Day 3 to 5 and 19 to 28 of lactation, and low levels from Day 7 to 16 of lactation. The results suggest that the induction of parturition by PGF 2α can influence the final stage of pregnancy and lactation period due to changes in plasma LH levels, and has no effect on mean plasma PRL and FSH levels during these same periods.

Inhibin-like activity in plasma from ovariectomized ewes and serum albumin: Pitfalls for radioimmunoassay

Progress to understand mechanisms that regulate inhibin secretion and action in farm animals has been handicapped by the shortage of simple, accurate assay methods to quantify inhibin in circulation. RIA would seem to provide the needed quantitative capability, but results of the following studies using inhibin RIA procedures reveal reasons to interpret inhibin immunological potency estimates with caution. Two sets of inhibin RIA reagents and various assay buffers were used. Initially, inhibin immunoactivity was estimated with an antiserum to a 32 amino acid peptide fragment from the alpha subunit of porcine inhibin [pIα(1–32)] and tracer to the peptide with tyrosine added in position 0 to permit radioiodination, pIα(0Tyr1–32). Later, an antiserum to pIα(1–29Tyr30) peptide and pIα(1–29Tyr30) tracer was evaluated as were several combinations of assay buffer and assay conditions. Both sets of assay reagents provided quantitative recovery of pIα(1–32) peptide from plasma, parallel response between the peptide and either ovine or bovine plasma, as well as adequate sensitivity to measure inhibin immunoactivity in 25 μl of plasma. However, plasma from long-term ovariectomized female sheep, swine or cattle appeared to contain nearly as much inhibin immunoactivity as intact animals. To explore the possibility that the adrenals may produce sufficient inhibin to account for unexplained high levels of inhibin immunoactivity in plasma from ovariectomized animals, ewes on days 12 and 13 of the estrous cycle were injected with either corn oil (CONT) or large doss of an adrenal steroid agonist, dexamethasone (DEX), to alter adrenal function. Likewise, ewes were either ovariectomized (OVX) on day 12 or injected on days 12 and 13 with estradiol-17β plus progesterone (E2+P4) to alter ovarian function. The plasma concentration of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) increased following ovariectomy (P<.001), and LH decreased following ovarian steroids (P<.001). Treatment with DEX did not change plasma gonadotropin values (P>.1). When plasma was assayed using pIα(1–32) reagents and an assay buffer consisting of gelatin/phosphate/Tween-20 (Ge1T20), inhibin immunoactivity was not affected by any of the four treatments (P>.1), even including ovariectomy. Re-assay of these same samples with an RIA procedure that used ge1T20 assay buffer and pIα(1–29Tyr30) reagents produced good agreement with the previous assay (partial correlation P<.0001), but there was no statistical evidence that ovariectomy or treatment with ovarian or adrenal steroids changed the level of immunoassayable inhibin in plasma. When plasma samples were re-assayed using BSA and .1% Triton-X-100 in the assay buffer, a significant decline in inhibin immunoactivity was detected at 2 hr following ovariectomy, but the overall effect of ovariectomy was not significant. Various RIA buffers were evaluated using the 1–32 peptide assay system. Binding of radiolabeled pIα(0Tyr1–32) to antibody was significantly inhibited (P<.01) by serum albumin (SA) from sheep, cattle or pigs. Also, inhibition of binding with SA, inhibin peptides and plasma from sheep, cattle and swine all appeared parallel. The large inhibin-like effect of plasma from ovariectomized animals and the unpredictable effects of proteins and detergents in assay buffer on both assays suggest that studies to describe the physiological control and function of inhibin in farm animals using these RIAs must be interpreted with extreme care.

Effect of recombinant human erythropoietin on anterior pituitary function in patients on chronic hemodialysis.

In 7 patients with end stage renal failure, anterior pituitary function was tested by simultaneous application of maximally effective doses of the hypothalamic releasing peptides, corticotropin-releasing hormone, growth hormone-releasing hormone, thyrotropin-releasing hormone and gonadotropin-releasing hormone, and compared to 8 normal controls. In addition to the pituitary hormones, plasma cortisol, thyroxine and testosterone concentrations were measured. To test for possible effects of treatment with recombinant human erythropoietin (rhu-EPO), all patients with chronic renal failure were studied again after partial correction of anemia by treatment with erythropoietin. Before initiation of rhu-EPO treatment, plasma concentrations of follicle-stimulating hormone were significantly elevated and the thyroid-stimulating hormone and prolactin responses to thyrotropin-releasing hormone blunted when compared to normal controls. Treatment with rhu-EPO induced a significant increase in plasma ACTH and follicle-stimulating hormone concentrations. All other pituitary functions remained unchanged. Thus, the general improvement in well-being, working capacity and sexual activity cannot be attributed to hormonal changes.

Acute Testicular Toxicity of 1,3-Dinitrobenzene and Ethylene Glycol Monomethyl Ether in the Rat: Evaluation of Biochemical Effect Markers and Hormonal Responses

The studies described in this paper were undertaken to evaluate the use of plasma enzymes of testicular origin and plasma hormones as markers of acute testicular toxicity. Rats were dosed by gavage with a single dose of either 1,3-d'nitrobenzene (1,3-DNB) or ethylene glycol monomethyl ether (EGME). Two experimental designs were used: a dose response and a time-dose response course. Lactate dehydrogenase isozyme C4 (LDH-C4) and sorbitol dehydrogenase (SDH) were used as germ cell markers and leucine aminotransferase (LAT) and androgen binding protein (ABP) were used as Sertoli cell markers. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone were also monitored. Histopathology confirmed the known testicular toxicity of 1,3-DNB and EGME. 1,3-DNB induced Sertoli cell damage with associated degenerative changes in late pachytene spermatocytes. The effects of EGME were mainly on early and late pachytene and dividing spermatocytes. No changes in either testicular or plasma SDH or LAT were found. Similarly no effects were observed for plasma LH or testosterone. However testicular LDH-C4 and testosterone, plasma LDH-Q, ABP, and FSH did show compound related effects. LDH-C4 was reduced in testis and increased in plasma with both compounds and plasma LDH-C4 remained elevated up to 14 days after dosing. ABP levels in plasma were increased with 1,3-DNB and EGME. A reduction in testicular testosterone levels was recorded and plasma FSH concentrations were elevated after EGME treatment. It is concluded that plasma LDH-C4 activity and ABP may be of diagnostic value in acute testicular toxicity. Increases in plasma LDH-C4 precede noticeable histological findings.

Acute testicular toxicity of 1,3-dinitrobenzene and ethylene glycol monomethyl ether in the rat: Evaluation of biochemical effect markers and hormonal responses

The studies described in this paper were undertaken to evaluate the use of plasma enzymes of testicular origin and plasma hormones as markers of acute testicular toxicity. Rats were dosed by gavage with a single dose of either 1,3-dinitrobenzene (1,3-DNB) or ethylene glycol monomethyl ether (EGME). Two experimental designs were used: a dose response and a time-dose response course. Lactate dehydrogenase isozyme C 4 (LDH-C 4) and sorbitol dehydrogenase (SDH) were used as germ cell markers and leucine aminotransferase (LAT) and androgen binding protein (ABP) were used as Sertoli cell markers. Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone were also monitored. Histopathology confirmed the known testicular toxicity of 1,3-DNB and EGME. 1,3-DNB induced Sertoli cell damage with associated degenerative changes in late pachytene spermatocytes. The effects of EGME were mainly on early and late pachytene and dividing spermatocytes. No changes in either testicular or plasma SDH or LAT were found. Similarly no effects were observed for plasma LH or testosterone. However testicular LDH-C 4 and testosterone, plasma LDH-C 4, ABP, and FSH did show compound related effects. LDH-C 4 was reduced in testis and increased in plasma with both compounds and plasma LDH-C 4 remained elevated up to 14 days after dosing. ABP levels in plasma were increased with 1,3-DNB and EGME. A reduction in testicular testosterone levels was recorded and plasma FSH concentrations were elevated after EGME treatment. It is concluded that plasma LDH-C 4 activity and ABP may be of diagnostic value in acute testicular toxicity. Increases in plasma LDH-C 4 precede noticeable histological findings.

The effect of various drugs with neuroendocrine activity and transdermal estradiol on plasma gonadotropin concentrations after ovariectomy in reproductive-aged women

In the present study we compared the effect of different neuroactive drugs with that of estrogen treatment on the ovariectomy-induced plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) changes. A total of 35 menstruating women undergoing ovariectomy were randomly divided into five groups of 7 patients each, receiving a 4-week treatment with oral clonidine, lisuride and sodium valproate, transdermal 17 beta-estradiol, or placebo. The treatment started the day after ovariectomy. Surgery was done during the early follicular phase of the cycle. Blood samples were collected before and after 3, 5, 7, 14, 21 and 28 days of treatment. During the treatment, hot flushes were subjectively recorded. The placebo-treated group showed a progressive increase in plasma LH and FSH concentration during the month following ovariectomy. The same changes occurred in the lisuride and sodium valproate treated groups. Plasma LH levels in ovariectomized women treated with clonidine showed an increase which was higher than in placebo-treated women (p less than 0.01), while FSH levels were similar to those in the placebo group. In the estradiol-treated group the increase in both gonadotropins was significantly less (p less than 0.01) than in the placebo group. The frequency and intensity of hot flushes were high in placebo and sodium valproate treated subjects, being significantly reduced by clonidine, lisuride and estrogen treatment. Our results seem to indicate that clonidine treatment modulates the LH postcastration rise and that both neuroendocrine and gonadal mechanisms influence the changes in the activity of the GnRH-pituitary axis following ovariectomy.

The ovarian follicle and fertility

The precise roles of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in the control of preovulatory follicle growth has been re-examined. Suppression of both pulsatile LH secretion and FSH or specific suppression of FSH results in an inhibition of preovulatory follicle growth beyond 2.5 mm dia. Infusion of sheep FSH alone in physiological amounts in the presence of basal, non-pulsatile LH results in the growth of preovulatory follicles. Co-infusion of large pulses of LH reduced or abolished this effect of FSH. It is suggested that: (1) FSH controls the number of follicles which develop; (2) selection of the large follicle destined to ovulate is directly related to the decline in the plasma concentration of FSH occurring during the period of follicle selection—thus, only the follicle(s) which can withstand this withdrawal of FSH will continue to develop; and (3) pulses of LH may directly affect the action of FSH on the follicle and play an important, hitherto unrecognized role in the selection of the ovulatory follicle by actively inducing atresia.

Pituitary Binding Sites for Gonadotrophin‐Releasing Hormone in Booroola Merino Ewes which were Non‐Carriers or Homozygotes of the Fecundity Gene F

Abstract Pituitary binding sites for gonadotrophin-releasing hormone (GnRH) were examined in Booroola ewes on Days 4 and 12 of the oestrous cycle and more than 12 months after ovariectomy. No significant differences were observed in the affinity of the binding sites for [(125) I]D Ala6, des Gly(10) GnRH ethylamide, in non-carriers (++) or homozygotes of the fecundity gene (FF), in intact or ovariectomized animals (overall K(a)= (1.8 +/- 0.1) x 10(9) M(-1); mean +/- SEM, n = 67). In ++ ewes, the number of GnRH binding sites on Day 4 of the oestrous cycle (0.199 +/- 0.025 fmol/mg pituitary, n = 8) was significantly greater (P<0.05) than on Day 12 (0.107 +/- 0.012 fmol/mg pituitary, n = 12). In contrast in FF ewes the number of binding sites on Days 4 and 12 were similar (Day 4: 0.119 +/- 0.030, n = 8; Day 12: 0.092 +/- 0.014, n = 10). On Day 4, but not Day 12, the binding site numbers were significantly higher in ++ compared with FF pituitaries (P<0.05). Likewise on Day 4, but not Day 12, the plasma concentrations of follicle-stimulating hormone were significantly higher (P<0.005) in FF (1.60 +/- 0.15 ng/ml) than ++ ewes (0.96 +/- 0.10 ng/ml). After ovariectomy, no gene-specific differences in binding site numbers were noted despite significantly higher plasma follicle-stimulating hormone concentrations in FF animals. No gene-specific differences in plasma luteinizing hormone concentrations were observed in these animals on Days 4 or 12, or after ovariectomy. Moreover, luteal phase plasma progesterone concentrations were also similar between ++ and FF ewes. We conclude that the gene-specific differences in pituitary responsiveness to GnRH and in pituitary gonadotrophin output are unlikely to be due to differences in GnRH receptor binding affinities.

Sex-related differences in the control of gonadotropin concentrations in neonatal pigs

Two experiments were conducted to examine gonadal regulation of gonadotropin secretion in male and female neonatal piglets. In the first experiment, a single i.p. injection of charcoal-treated porcine follicular fluid (pFF) lowered ( P < 0.05) concentrations of plasma follicle-stimulating hormone (FSH) at 6 and 12 h after administration in 7-day-old intact male piglets, but failed to alter FSH in castrated male or intact female piglets. In the second experiment, administration of pFF twice daily from day 0 to 14 of life caused an increase in plasma FSH levels in intact males, but did not significantly alter FSH in females or in males castrated at birth. Plasma LH did not differ between male and female piglets, but FSH was significantly lower in males than in females. Castration of males at birth resulted in lower testosterone and estradiol-17β levels and resulted in a gradual increase in concentrations of FSH over the 14-day experimental period. Treatment of neonatal pigs with pFF altered concentrations of FSH in intact males, but not in intact females, indicating a divergence between the sexes in the postnatal control of FSH secretion.

Alterations in Gonadotropin Secretion and Ovarian Function in Prepubertal Gilts by Elevated Environmental Temperature1

The effect of chronic exposure to elevated environmental temperature on gonadotropin secretion and ovarian function was studied in prepubertal gilts. Gilts were maintained under control (15.6 degrees C) or elevated temperature (33.3 degrees C) conditions from 150 to 180 days of age. Endocrine and ovarian responses to bilateral (BLO), unilateral (ULO), and sham ovariectomy were evaluated between 175 and 180 days of age. During the 96-h sampling period after BLO, plasma concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were suppressed in heat-stressed females. Similarly, elevated temperatures abolished the transient rise in FSH and subsequent follicular growth normally associated with ULO. In contrast, environmental treatment had no effect on the secretion of FSH and LH after sham ovariectomy, yet the number of small follicles was lower in gilts exposed to elevated temperatures than in females maintained under control conditions. These results indicate that a chronic exposure to elevated environmental temperature during pubertal development diminished the ability of the hypothalamo-hypophyseal axis to secrete FSH and LH, which had physiological consequences on follicular growth. When provided an appropriate stimulus (ULO), an acute period of FSH secretion and subsequent development of follicles failed to occur in females exposed to elevated temperatures. Consequently, we propose that delayed puberty in gilts during periods of elevated environmental temperatures is due, in part, to a diminished capacity for gonadotropin secretion.

Changes in peripheral levels of immunoreactive inhibin and gonadotropins in cattle induced to superovulate by porcine follicle-stimulating hormone.

Concentrations of inhibin in peripheral blood were determined in cattle treated with porcine follicle-stimulating hormone (FSH). Changes in plasma concentrations of FSH, luteinizing hormone (LH), estradiol and progesterone were also examined. These results were compared with hormonal profiles in the intact estrous cycle prior to FSH treatment of the same cows. Plasma levels of estradiol before ovulation and of progesterone after ovulation during the period of treatment with porcine FSH were much higher than those in the intact cycle. Concentrations of plasma inhibin rose promptly after injections of porcine FSH and maintained high levels for a longer period than estradiol after the LH surge. Changes in plasma concentrations of inhibin were not correlated to those of progesterone in superovulating cattle. In the superovulating animals, peaks of the preovulatory FSH surge were suppressed to 70.4% of the intact cycle, though LH peaks were not significantly suppressed. These results indicate that high levels of inhibin after treatment with porcine FSH may be involved in a partial suppression of the preovulatory surge of FSH in superovulating cattle. These findings also suggest that unovulated follicles maintain the ability to secrete inhibin and that the corpus luteum in superovulating cattle is not the active source of inhibin secretion.

Role of Substance P in the Medial Preoptic Area in the Regulation of Gonadotropin and Prolactin Secretion in Normal or Orchidectomized Rats

The present studies were designed to evaluate the role of substance P (SP) in the control of the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL). SP was microinjected into the medial preoptic area (MPOA) of conscious, freely moving intact or orchidectomized (ORCX; 21 days post-ORCX) adult male rats. Microinjection of SP into the MPOA induced a significant decrease in plasma LH and FSH concentrations, effects which were accompanied by an elevation in plasma PRL concentration. To examine the participation of endogenously secreted SP in the activity of the MPOA neurons controlling release of these cited pituitary hormones, another study was performed in which either a potent and specific antagonist to SP (D-Pro2, D-Trip7,9-SP; SP-ANT) or an antibody against SP (SP-AB), was injected into the MPOA. SP-ANT and SP-AB both elevated plasma LH, FSH and decreased plasma PRL concentration. These data suggest that endogenous SP within the MPOA exerts an important inhibitory tonus over LH and FSH release and an excitatory tonus over PRL release. In conclusion, SP seems to participate as a neurotransmitter or neuromodulater in the control of LH, FSH and PRL secretion, at least in part, by acting at the level of MPOA, a region in which the neuronal cell bodies that produce LH-releasing hormone and the associated gonadotropin-releasing hormone-associated peptide are located.

The effect of pregnant mare serum gonadotropin on follicle stimulating hormone and estradiol secretion in the prepuberal gilt

The effect of pregnant mare serum gonadotropin (PMSG) on follicle stimulating hormone (FSH) and estradiol concentrations was studied in 14 prepuberal gilts. At 157 ± 3 days of age, gilts were randomly assigned to receive a single subcutaneous injection of either saline (C; n = 7) or 1000 IU of PMSG ( n = 7). Treatments were administered at 08.00 h. Blood was collected on days −2, −1, 0, 1, 2, 3 and 4 (day 0 = day of injection). Samples were taken at 15-min intervals between 08.00 and 12.00 h and 20.00 h and 24.00 h. Additional samples were taken every 2.67 h between 24.00 and 08.00 h and 12.00 and 20.00 h. Concentrations of FSH during the preinjection period were similar ( P < 0.05) between the two treatments (C; 4.4 ± 0.5 vs PMSG; 4.5 ± 0.7 ng/ml). Mean plasma concentrations of FSH post injection were 4.8 ± 0.9 and 3.4 ± 0.8 ng/ml in C and PMSG gilts, respectively, and were not different ( P > 0.05). Mean daily FSH concentrations decreased ( P < 0.06) from 4.4 ± 0.06 ng/ml on day 0 to 2.6 ± 0.7 ng/ml on day 4 in PMSG gilts. Mean daily concentrations of estradiol were higher ( P < 0.05) on days 2, 3 and 4 in gilts receiving PMSG when compared to C females. Laparoscopic examination of the ovaries on day 6 revealed that the PMSG-treated gilts had ovulated while the C gilts did not. These results indicate that PMSG stimulated follicular growth and ovulation in prepuberal gilts with no increase in plasma concentrations of FSH.

Regulation of Anterior Pituitary Gonadotrophin Subunit mRNA Levels by Gonadotrophin‐Releasing Hormone in the Ewe

Abstract Levels of mRNA for the common a subunit and for the beta subunits of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured in the pituitary glands of ovariectomized hypothalamo-pituitary disconnected ewes. A control group (n = 7) received 250 ng pulses of gonadotrophin-releasing hormone (GnRH) each hour for one week. To examine the effects of changing GnRH pulse amplitude four sheep were given 250 ng pulses of GnRH for one week and then 25 ng pulses for one week. Plasma LH and FSH concentrations were lowered by reducing the GnRH pulse amplitude but pituitary levels of mRNA for a subunit were increased. Levels of mRNA for FSHbeta and LHbeta were similar with 25 ng and 250 ng pulses of GnRH. To examine the importance of pulsatile versus continuous GnRH inputs, a group of sheep was given a constant infusion of 250 ng/h GnRH for one week. Compared to sheep given 250 ng pulses of GnRH the mRNA levels for LHbeta and FSHbeta were lower in sheep given a constant infusion of GnRH; levels of a subunit mRNA were similar in the two groups. To examine the short-term effects of removing GnRH inputs, ovariectomized, hypothalamo-pituitary disconnected ewes that had been receiving 250 ng pulses of GnRH each hour were deprived of GnRH for 6 h (n = 4) or 30 h prior to slaughter; levels of mRNA for the three subunits were similar to control values in both of these groups. These studies show that wide variation in GnRH pulse amplitude has little effect on mRNA levels for the gonadotrophin subunits but message levels are affected by the mode of GnRH input (constant versus pulsatile). The maintenance of gonadotrophin subunit mRNA levels for at least 30 h after GnRH deprivation suggests that these mRNA species have a long half-life or that transcription continues after GnRH withdrawal.

Periovulatory Endocrinology and Oocyte Maturation in Unmated Mature Blue Fox Vixens (Alopex lagopus)

Nine of 10 mature blue fox vixens (Alopex lagopus) in spontaneous oestrus ovulated approximately 2 days after the preovulatory increase in luteinizing hormone (LH). Plasma concentrations of follicle-stimulating hormone and progesterone increased simultaneously with the LH peak, whereas oestradiol-17 beta peaked 1 day previously. In the tenth vixen, an LH peak was not observed, and neither visible follicles nor corpora lutea were found in the ovaries 6 days after peak vaginal electrical resistance. Eggs were ovulated as primary oocytes, but oocyte maturation was initiated within the day of ovulation (2 days after the LH peak). Within the next 2 days (3-4 days after the LH peak) the first polar body was extruded, and the cumulus mass was completely dissociated from the zona pellucida. The interval between the preovulatory LH peak and initiation of the final oocyte maturation is thus considerably longer in the blue fox than for example in the cow (48-72 h compared with 9-12 h). This suggests that the relationship between these two events is somewhat different in the blue fox.

Plasma concentrations of pituitary hormones in 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐treated male rats

Experiments were conducted to test the hypothesis that acute TCDD toxicity is associated with pituitary hypofunction. Sexually mature male Sprague-Dawley rats were given graded doses of TCDD (0-100 micrograms/kg) and evaluated 7 days later. Despite pronounced hypophagia and body weight loss, plasma concentrations of growth hormone (GH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) were not significantly affected by any dose of TCDD. Only prolactin (PRL) concentrations were reduced, while, as previously reported, thyroid-stimulating hormone concentrations were elevated. Also, plasma LH, PRL, and adrenocorticotropic hormone (ACTH) concentrations were not significantly affected 1, 2, 3, 4, 5, or 7 days after a single dose of TCDD (50 micrograms/kg). We conclude that (1) pituitary hypofunction is not a major cause of the initial stages of acute TCDD toxicity, (2) growth retardation in TCDD-treated rats is not the result of a deficiency of GH, (3) alterations in plasma corticosterone concentrations are due to altered responsiveness of the adrenal to ACTH stimulation rather than to changes in plasma ACTH concentrations, and (4) that impaired spermatogenesis is not associated with a decrease in plasma FSH concentrations. In addition, the lack of a consistent effect on plasma PRL concentrations suggests that alterations in plasma PRL concentrations do not play a critical role in the toxicity of TCDD. Finally, because TCDD treatment causes a serious androgenic deficiency without increasing the rates at which androgens are catabolized or excreted, the fact that plasma LH concentrations were unaffected indicates that TCDD treatment must reduce the responsiveness of the testis to LH stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Suppression of gonadotrophin secretion does not reverse premature ovarian failure

The effect of prolonged inhibition of gonadotrophin secretion was studied in 12 women with premature ovarian failure. All the patients had plasma concentrations of follicle-stimulating hormone (FSH) greater than 20 i.u./l, and in six, primordial follicles had been seen on ovarian biopsy. Goserelin (Zoladex, ICI), a depot synthetic analogue of luteinizing hormone-releasing hormone (LHRH) was administered by three consecutive 4-weekly injections. Plasma concentrations of luteinizing hormone (LH) fell from 34 (SD 11) i.u./l to 2.4 (SD 1.9) i.u./l, and plasma concentrations of FSH fell from 106 (SD 29) i.u./l to 4.5 (SD 2.6) i.u./l 4 weeks after the first injection. Plasma concentrations of gonadotrophins returned to pretreatment values in every patient within 9 weeks of the final injection of goserelin. Regular ultrasonography during the period following the final injection failed to demonstrate the development of ovarian follicles in any patient, and plasma concentrations of oestradiol remained below 100 pmol/l. This study has failed to show that suppression of gonadotrophin secretion reverses premature ovarian failure.

Effects of Bovine Follicular Fluid on Pulsatile Secretion of Gonadotrophin‐Releasing Hormone and Gonadotrophins in Ovariectomized Ewes

Abstract Ovariectomized ewes were injected with charcoal-extracted bovine follicular fluid (n = 5) or with hypophysectomized ewe serum (n = 5) after which hypophyseal portal blood samples were taken to monitor the release of gonadotrophin-releasing hormone (GnRH). Peripheral blood samples were also taken to monitor plasma luteinizing hormone and follicle-stimulating hormone (FSH) concentrations. Bovine follicular fluid treatment caused a 50% decrease in plasma FSH concentrations whereas hypophysectomized ewe serum did not significantly alter plasma FSH levels. The frequency and amplitude of luteinizing hormone and GnRH pulses was similar in both experimental groups. It is concluded that inhibin activity in bovine follicular fluid selectively suppresses the release of FSH by direct action on the pituitary gland, with no effect on GnRH secretion.

Ovarian inhibition of peripheral plasma concentration of follicle stimulating hormone in prepuberal holstein heifers

The objective of this study was to determine effects of age and castration on follicle stimulating hormone (FSH) secretion in prepuberal heifers. In experiment 1, twelve heifers were bilaterally ovariectomized at 3, 6, or 9 months of age (n = 4/group). Blood was collected at 10 min intervals for 8 hr at 1 week before ovariectomy and 1 and 4 weeks after ovariectomy. Frequency, amplitude and duration of FSH pulses were calculated. Mean plasma concentration of FSH (ng/ml), and frequency (pulses/8 hr), amplitude (ng/ml), and duration (min/pulse) of FSH pulses were not altered by age. Mean concentration of FSH increased (P<.01) from 1 week before to 1 week and 4 weeks after ovariectomy, respectively, in all age groups. Pulse frequency increased (P<.05) from 1 week before ovariectomy to 4 weeks after ovariectomy in 3 month old heifers. Pulse amplitude of FSH increased (P<.01) from 1 week before to 1 week after ovariectomy in 3 month old heifers, from 1 week before to 4 weeks after ovariectomy in 6 month old heifers, and from 1 week before to 1 week and 4 weeks after ovariectomy in 9 month old heifers. In experiment 2, twelve heifers were bilaterally ovariectomized at 3, 6 or 9 weeks of age (n = 4/group). Sample collection and measurement of mean concentration of FSH were the same as in experiment 1. Mean concentration of FSH increased (P<.01) from 1 week before to 1 and 4 weeks after ovariectomy in heifers ovariectomized at 6 and 9 weeks of age. Mean concentration of FSH increased (P<.01) from 1 week before to 4 weeks after ovariectomy in heifers ovariectomized at 3 weeks of age and was increasingly higher (P<.05) in heifers ovariectomized at 3 to 6 to 9 weeks of age. Thus, ovarian inhibition of FSH secretion is established in Holstein heifers ovariectomized at 9 weeks of age and maintained through 9 months of age.

Influence of germ cells upon Sertoli cells during continuous low-dose rate γ-irradiation of adult rats

The effects of continuous γ-irradiation of adult rats at two low-dose rates (7 cGy and 12 cGy/day; up to a total dose of 9.1 Gy and 10.69 Gy 60Co γ-ray, respectively) were investigated. Over a period of 3–131 days of irradiation, groups of experimental and control animals were killed. Body weight, testis, epididymis, prostate and seminal vesicle weights, the number of germ cells and Sertoli cells, tubular ultrastructure, epididymal and testicular levels of biologically active androgen-binding protein (ABP), and the plasma concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone were monitored. Irradiation had no effect on body weight, whereas testicular and epididymal weight began to decrease following 35 and 50 days of irradiation at 7 and 12 cGy, respectively. At 7 cGy the target cells of the γ-rays were essentially A spermatogonia, whereas at 12 cGy A spermatogonia and preleptotene spermatocytes were primarily affected. This resulted in a progressive and sequential dose-related reduction in the number of pachytene spermatocytes, round spermatids and late spermatids (LS). Under both irradiation procedures the Sertoli cell number remained unchanged whereas partial (7 cGy) or no change (12 cGy) was seen at the Leydig cell level. Whatever the irradiation protocol, from the time LS numbers decreased, vacuolisation of the Sertoli cell cytoplasm progressively occurred, followed by thickening and folding of the peritubular tissue. Moreover, in parallel to the drop in the number of these germ cell types, ABP production fell whereas FSH levels rose. A highly significant positive correlation was found between LS numbers and these Sertoli cell parameters. This study supports our previous concept of a control of certain important aspects of Sertoli cell function by late spermatids in the adult rat.