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PubMed1984

A comparison of the luteinizing hormone-releasing activities of synthetic chicken luteinizing hormone-releasing hormone (LH-RH), synthetic porcine LH-RH, and buserelin, an LH-RH analogue, in the domestic fowl.

The luteinizing hormone-releasing activities of synthetic chicken luteinizing hormone-releasing hormone (chLH-RH), synthetic porcine LH-RH (pLH-RH), and an analogue of LH-RH (buserelin, D-Ser-(But)6-des-Gly10-LH-RH ethylamide) were compared in the domestic fowl. In adult cockerels, intravenous injections of 0.5 or 1 microgram chLH-RH/kg released the same amount of LH as the same doses of pLH-RH; subcutaneous injections of 0.5 or 1 microgram buserelin/kg were about twice as effective as the same doses of pLH-RH. In laying hens, injections of 1, 10, 20, and 50 micrograms buserelin induced more sustained releases of LH than the corresponding doses of pLH-RH. Daily injections of 1 or 10 micrograms buserelin/bird or of 10 micrograms pLH-RH/bird for 12 days synchronized the timing of most ovipositions showing that the injections of releasing hormone could induce preovulatory surges of LH. In contrast with mammals, daily injections of buserelin in laying hens did not reduce pituitary responsiveness to the analogue. It is concluded that the structural difference between mammalian and chicken LH-RH does not affect their LH-releasing activities in the domestic fowl. Although the LH-releasing activity of buserelin in the hen is greater than that of pLH-RH, the difference in activity is not as great as that observed in most mammals. This view is strengthened by the finding that chronic treatment with buserelin, which exerts an antagonistic effect on ovulation in mammals, does not do so in the domestic hen.

Animals↗
PubMed1986

Comparison of mammalian luteinizing hormone releasing hormone (LH-RH), and of an analog (ICI 118630), on luteinizing hormone and ovarian steroid (progesterone, oestradiol) secretions in laying hens. (Gallus domesticus).

This experiment was conducted to compare the luteinizing hormone (LH), progesterone (P4) and oestradiol (E2) release in response to injections of various doses of synthetic mammalian luteinizing hormone-releasing hormone (LH-RH) and of an LH-RH agonist, ICI 118630, administered to laying hens 4 to 9 hours after a mid-sequence ovulation. Plasma LH increased significantly within 10 minutes of injection of either compound whereas any increases in plasma steroid concentrations were discerned later, at approximately minutes post-injection. No dose-response relationship was found for either compound with respect to LH release, but ICI 118630 appeared more potent than LH-RH. This analog also produced a greater mean incremental rise in plasma progesterone, but not oestradiol, than LH-RH, and this was found in animals injected at a time when the largest ovarian follicle was not mature. These result suggest that ICI 118630 is a more potent releasing hormone in the hen at the level of the pituitary, and that it may have a stimulating effect on ovarian progesterone secretion.

Animals↗
PubMed1980

Alteration in the normal pattern of serum testosterone and 5 alpha-androstane-3 alpha, 17 beta-diol in the immature male rat following chronic treatment with luteinizing hormone releasing hormone or luteinizing hormone.

A major component of sexual maturation in the male rat is a progressive decline in serum concentrations of 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) and a concomitant increase in testicular testosterone biosynthesis and secretion. Chronic administration of synthetic luteinizing hormone releasing hormone (LHRH) or luteinizing hormone (LH)/human chorionic gonadotropin (hCG) to immature male rats has been shown to result in a delay in sexual maturation as evidenced by decreased sex accessory gland weights and altered testicular testosterone production. We have examined the postulate that such treatments may either reverse or retard the normal developmental pattern of serum testosterone and 3 alpha-diol concentrations. Chronic in vivo treatment of 28 day old immature male rats for 2 weeks with daily injections of either 0.5 micrograms of LHRH, 1.0 micrograms of LHRH, or 30 micrograms of LH was found to result in significant reductions in weights of the seminal vesicles and ventral prostate glands and diminutions in serum testosterone concentrations. Serum content of 3 alpha-diol was either unchanged or slightly elevated in the LHRH treated animals and increased significantly in the LH treated animals. These data suggest that either a reversal of or retardation in the normal developmental pattern of serum testosterone and 3 alpha-diol content has been achieved in the immature male rat by chronic LHRH or LH treatment.

Androstane-3,17-diol↗
PubMed1991

Effect of luteinizing hormone releasing hormone pulse characteristics on comparative luteinizing hormone and follicle stimulating hormone secretion from superfused rat anterior pituitary cell cultures.

We have shown that 4 ng luteinizing hormone releasing hormone (LHRH) pulses induced significantly greater luteinizing hormone (LH) release from proestrous rat superfused anterior pituitary cells with no cycle related differences in follicle stimulating hormone (FSH). Current studies gave 8 ng LHRH in various pulse regimens to study amplitude, duration and frequency effects on LH and FSH secretion from estrous 0800, proestrous 1500 and proestrous 1900 cells. Regimen 1 gave 8 ng LHRH as a single bolus once/h; regimen 2 divided the 8 ng into 3 equal 'minipulses' given at 4 min intervals to extend duration; regimen 3 gave the 3 'minipulses' at 10 min intervals, thereby further extending duration: regimen 4 was the same as regimen 2, except that the 3 'minipulses' were given at a pulse frequency of 2 h rather than 1 h. In experiment 1, all four regimens were employed at proestrus 1900. FSH was significantly elevated by all 8 ng regimens as compared to 4 ng pulses; further, 8 ng divided into 3 equal 'minipulses' separated by 4 min at 1 and 3 h frequencies (regimens 2 and 4) resulted in FSH secretion that was significantly greater than with either a single 8 ng bolus (regimen 1) or when the 'minipulses' were separated by 10 min (regimen 3). In experiment 2, at proestrus 1500, FSH response to the second pulse of regimen 4 was significantly greater than in regimen 2; LH release was significantly suppressed at pulse 2 compared to regimen 2 accentuating divergent FSH secretion. At estrus 0800, FSH response to the second pulse of regimen 4 was significantly stimulated FSH at proestrus 1900, 1500 and estrus 0800, FSH divergence was most marked at proestrus 1500. These data indicate a potential role for hypothalamic LHRH secretory pattern in inducing divergent gonadotropin secretion in the rat.

Animals↗
PubMed1978

Dissociation of the porcine anterior pituitary: the kinetics of luteinizing hormone release in response to luteinizing hormone-releasing hormone.

A method has been developed for disaggregating porcine anterior pituitary tissue and for providing dissociated preparations which have good, stable viability in culture. The secretory capacity for these preparations in terms of their ability to release luteinizing hormone in response to luteinizing hormone-releasing hormone has been documented in detail. In following the short-term kinetics of LH secretion a biphasic pattern of release has been demonstrated in which a sharp initial peak, maximal at 2 min, is followed by a second, more prolonged phase of release reaching a maximum between 10 and 20 min.

Animals↗
PubMed1979

Interaction of luteinizing hormone-releasing hormone, cyproterone acetate and arginine vasotocin on plasma levels of luteinizing hormone in intact and castrated adult male rats.

Treatment of unanesthetized castrated adult male rats every 3 h for 48 h with either 5 microgram of arginine vasotocin (AVT) and/or 1 microgram luteinizing hormone-releasing hormone (LRH) caused a significant inhibition of plasma levels of luteinizing hormone (LH) and compared to castrated control rats receiving diluent only. However, the intravenous (iv) injection of 1 microgram of AVT into urethane-anesthetized male rats which had been castrated for 0, 24 or 48 h did not affect plasma levels of LH at 10, 20 or 60 min following injection compared to their respective diluent-treated castrated control rats. Similarly, the iv injection of either 100 ng, 1 microgram or 10 microgram AVT was unable to acutely affect plasma levels of LH in intact male rats. Following the iv injection of 2 doses of 50 ng LRH spaced 1 h apart in anesthetized castrated male rats, 2 peaks of equal magnitude in plasma LH were noted. Castrated rats treated with 2 injections spaced 1 h apart of LRH + AVT had significantly higher plasma levels of LH than did rats treated with LRH alone. In subsequent studies, both AVT and arginine vasopressin were observed to augment the plasma response of LH to an injection of LRH whereas oxytocin had no effect. A single injection of AVT + LRH significantly augmented the plasma titers of LH compared to levels observed in LRH-treated control rats as did a second injection 1 h later. The administration of cyproterone acetate sc for 2 days by itself had no effect on plasma LH but in conjunction with LRH caused a marked rise in plasma LH compared to intact rats treated with LRH alone. AVT in combination with LRH and cyproterone acetate caused a significant elevation in plasma LH at 60 min post-injection when compared to plasma levels of rats treated with LRH alone or the combination of LRH and cyproterone acetate. It is concluded that acute intravenous injections of AVT augment the LH-releasing activity of LRH; chronic treatment for 48 h, however, with LRH + AVT leads to a significant depression of plasma LH perhaps due to an exhaustion of the releasable pool of LH in the anterior pituitary.

Animals↗
PubMed1986

Nicotine-induced increases in brain luteinizing hormone releasing hormone-like immunoreactivity and in serum luteinizing hormone levels of the male rat.

By means of radioimmunoassay procedures luteinizing hormone releasing hormone (LHRH)-, Metenkephalin- and somatostatin-like immunoreactivities have been measured in discrete hypothalamic and preoptic nuclei as well as serum luteinizing hormone (LH) levels. Nicotine (2 mg/kg, i.p.) produced after 5 min a significant and selective increase in LHRH-like immunoreactivity in the median eminence and in the medial preoptic nucleus, associated with increases in serum LH levels but without any changes in Met-enkephalin and somatostatin-like immunoreactivities in the median eminence. The results indicate that the nicotine-induced activation of LHRH-immunoreactive neurons involves an enhanced processing of the precursor peptide to LHRH.

Animals↗
PubMed1995

Agmatine, a novel hypothalamic amine, stimulates pituitary luteinizing hormone release in vivo and hypothalamic luteinizing hormone-releasing hormone release in vitro.

Agmatine, a clonidine displacing substance and imidazoline receptor agonist, was recently isolated from bovine brain and shown to be present in the rat hypothalamus. Since clonidine can stimulate the release of pituitary luteinizing hormone (LH), we tested the hypothesis that agmatine may similarly act in the rat to stimulate the hypothalamic luteinizing hormone-releasing hormone (LHRH)-pituitary LH axis. Administration of agmatine intracerebroventricularly rapidly augmented the release of LH in a dose-related fashion in ovariectomized, ovarian steroid-primed rats. Additionally, agmatine enhanced the in vitro efflux of LH releasing hormone from the median eminence-arcuate nucleus of the hypothalami of rats similarly pretreated with steroids. These studies imply that the endogenous imidazoline receptor agonist, agmatine, may serve as an excitatory neurotransmitter/neuromodulator in the hypothalamic control of LH release and we suggest that the previously reported excitatory effects of clonidine on LH release may be attributed to stimulation by clonidine of imidazoline receptors.

Agmatine↗
PubMed1992

Associated luteinizing hormone-releasing hormone and luteinizing hormone secretion in ovariectomized gilts.

The secretion of luteinizing hormone-releasing hormone (LHRH) and its temporal association with pulses of luteinizing hormone (LH) was examined in ovariectomized prepuberal gilts. Push-pull cannulae (PPC) were implanted within the anterior pituitary gland and LHRH was quantified from 10 min (200 microliters) perfusate samples. Serum LH concentrations were determined from jugular vein blood obtained at the midpoint of perfusate collection. Initial studies without collection of blood samples, indicated that LHRH secretion in the ovariectomized gilt was pulsatile with pulses comprised of one to three samples. However, most pulses were probably of rapid onset and short duration, since they comprised only one sample. Greater LHRH pulse amplitudes were associated with PPC locations within medial regions of the anterior pituitary close to the median eminence. In studies which involved blood collection, LH secretion was not affected by push-pull perfusion of the anterior pituitary gland in most gilts, however, adaptation of pigs to the sampling procedures was essential for prolonged sampling. There was a close temporal relationship between perfusate LHRH pulses and serum LH pulses with LHRH pulses occurring coincident or one sample preceding serum LH pulses. There were occasional LHRH pulses without LH pulses and LH pulses without detectable LHRH pulses. These results provide direct evidence that pulsatile LHRH secretion is associated with pulsatile LH secretion in ovariectomized gilts. In addition, PPC perfusion of the anterior pituitary is a viable procedure for assessing hypothalamic hypophyseal neurohormone relationships.

Animals↗
PubMed1981

Long-term effect of D-Trp6-luteinizing hormone-releasing hormone on testicular size and luteinizing hormone, follicle-stimulating hormone, and testosterone levels in hypothalamic hypogonadotropic males.

Six men, ages 18 to 34 years, with hypothalamic hypogonadotropism were treated with D-Trp6-luteinizing hormone-releasing hormone (10 micrograms intramuscularly on alternate days) for a period of 6 months. They underwent an intravenous luteinizing hormone-releasing hormone (LH-RH) test (50 micrograms/sq m) before and after 1, 3, and 6 months of treatment. During the first 3 months of therapy, the mean (+/- standard deviation) testicular volume increased from 3.5 +/- 1.0 ml to 6.0 +/- 2.0 ml, but decreased to 5.0 +/- 1.0 ml after 6 months. A significant increase in the plasma LH response to LH-RH over pretreatment levels was noted after 1 month (10.2 +/- 4.2 mIU/ml versus 1.6 +/- 1.0 mIU/ml, P less than 0.001) and 3 months (3.0 +/- 1.6 mIU/ml, P less than 0.01) with a subsequent decline to pretreatment levels after 6 months of treatment. The follicle-stimulating hormone response to LH-RH was not significant. It is concluded that D-Trp6-LH-RH induced an initial stimulation in these patients but, probably because of the excessively high dose used, a paradoxical inhibitory response was obtained after 3 months of therapy.

Adolescent↗
PubMed1981

Inhibition of the postcastration rise of luteinizing hormone and follicle-stimulating hormone in female rhesus monkeys (Macaca mulatta) by the administration of a luteinizing hormone-releasing hormone inhibitory analog ([N-Ac-D-Trp1-3,D-p-Cl-phe2,D-Phe6,D-Ala10]-LH-RH).

Regularly cycling rhesus monkeys were bilaterally oophorectomized for study of postcastration rise of follicle-stimulating hormone (FSH) and luteinizing hormone (LH). The animals were divided in two groups, control animals, which received vehicle, and experimental animals, which received intramuscularly 1 mg of a potent luteinizing hormone-releasing hormone (LHRH) inhibitory analog ([N-Ac-D-Trp1-3,D-p-Cl-phe2,D-Phe6,D-Ala10]-LH-RH) from the day of castration for 10 days. The controls showed significant elevations of FSH and LH 3 to 4 days after castration, but in the experimental animals the rise in gonadotropins was blocked until the LHRH antagonist administration was discontinued. The dynamics of gonadotropin elevation after the discontinuation of [N-Ac-D-Trp1-3,D-p-Cl-phe2,D-Phe6,D-Ala10]-LH-RH administration were similar to those observed in control animals after castration. The availability of a compound that selectively inhibits FSH and LH secretion in primates opens a new approach to contraception and for the treatment of conditions in which gonadotropin inhibition is desired.

Animals↗
PubMed1983

Gonadotroph and corpus luteum responses to two successive intranasal doses of a luteinizing hormone-releasing hormone agonist at different days after the midcycle luteinizing hormone surge.

Two successive intranasal doses (300 micrograms at 8:00 A.M. and 6:00 P.M.) of the luteinizing hormone-releasing hormone (LH-RH) agonist (D-Ser[TBU]6-des-Gly-NH2(10))LH-RH ethylamide (Buserelin) were administered on days 1 to 10 after the midcycle luteinizing hormone (LH) surge in 33 normally cycling women. Maximal stimulation of gonadotropins was observed at 4 hours and was of higher amplitude in the first 2 days after the LH surge. The response to the second dose was markedly blunted, showing pituitary refractoriness. On each day of treatment there was a progressive increase of serum estradiol, which was maximal (threefold) 4 hours after the second dose of Buserelin. Serum progesterone (P) levels were not significantly changed on days 1 to 4, but they were increased by 50% at 10 hours on days 5 to 10. Daily blood samples revealed that following treatment on days 1 to 4 after the midcycle LH surge, serum P profiles were lower than in control cycles, without change in the length of the luteal phase. Starting on treatment day 5, a precocious luteolysis was induced, as illustrated by an early fall in serum P levels and shortening of the luteal phase (1 to 4 days). All posttreatment control cycles were normal. The results of this time study indicate that an appropriate treatment with an intranasal Buserelin administered at any time between days 1 to 10 after the midcycle LH surge impair luteal function and could lead to a new postcoital contraceptive approach.

Administration, Intranasal↗
PubMed1983

The effect of pulsatile and continuous intravenous luteinizing hormone-releasing hormone administration on pituitary luteinizing hormone and follicle-stimulating hormone release in normal men.

In 14 healthy, potentially fertile men, pituitary gonadotropin responses were studied under standardized conditions. Luteinizing hormone-releasing hormone (LH-RH) was given as a continuous infusion of 1 microgram/minute for 4 hours or in a pulsatile fashion with 20 micrograms as an intravenous bolus at intervals of 20 minutes for 4 hours. Blood was collected continuously by means of an integrated sampling technique. The mean serum luteinizing hormone (LH) concentration showed an oscillating pattern around a plateau level reached within 45 minutes during continuous LH-RH administration. During pulsatile infusion, an identical pattern for the first 45 minutes was observed with, thereafter, a continuous increase from 105 minutes until the end of the infusion. The mean increase in the serum LH level during pulsatile administration was significantly higher (P = 0.00001) than the mean increase seen during continuous infusion. The follicle-stimulating hormone concentration revealed a gradual progressive increase after both methods of stimulation, without a significant difference in the mean increase between the two types of administration. This study demonstrates the existence of a self-priming effect of LH after pulsatile LH-RH administration in the man like that in the woman.

Adult↗
PubMed1985

Depressed follicle-stimulating hormone, luteinizing hormone, and prolactin responses to the luteinizing hormone-releasing hormone, thyrotropin-releasing hormone, and metoclopramide test in endurance runners in the hard-training season.

The responses of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) to luteinizing hormone-releasing hormone (LH-RH) and the responses of prolactin (PRL) to thyrotropin-releasing hormone (TRH) and metoclopramide (MC) were measured in the late luteal phase of the cycle in 12 endurance runners and 11 control women and in 12 joggers and 7 control women. LH-RH (100 micrograms) and TRH (200 micrograms) were injected intravenously at the beginning of the test, and MC (10 mg) was injected 60 minutes later. Blood samples were obtained before and 20, 60, 80, and 120 minutes after the beginning of the test. Runners had significantly lower serum concentrations of estradiol and progesterone than control subjects, whereas the concentrations of FSH, LH, and PRL were similar at the beginning of the study. Compared with their controls, the runners had significantly lower FSH (P less than 0.05) and LH responses at 20 minutes (P less than 0.05) and lower LH responses at 80 minutes (P less than 0.01) to LH-RH and lower PRL responses to MC 20 minutes after MC injection (P less than 0.05). Joggers and their control subjects had similar LH, FSH, and PRL responses to these pharmacologic stimuli. It is concluded that decreased ovarian activity explains, at least partly, the lowered responses of FSH and LH to LH-RH and the lowered response of PRL to MC in endurance runners.

Estradiol↗
PubMed1989

Luteinizing hormone responses to luteinizing hormone releasing hormone (LHRH) in acute mania and the effects of lithium on LHRH and thyrotrophin releasing hormone tests in volunteers.

The endocrine responses to Luteinizing Hormone Releasing Hormone (LHRH) of eight drug-free males with mania were determined. Basal levels of Luteinizing Hormone (LH) and the plasma levels following injection of LHRH were elevated in patients compared with controls; Follicle Stimulating Hormone (FSH) and testosterone were not different. Elevated levels of LH have been described previously in recovered manic patients and have been suggested to be state-independent features of mania. In order to clarify the status of this finding, the effects of lithium administration upon hormone responses to LHRH in six male volunteers were also investigated, together with the effects upon Thyrotrophin Releasing Hormone (TRH) stimulation of Thyroid Stimulating Hormone (TSH) and prolactin release. Lithium increased the basal levels of LH and levels after injection of LHRH without effect upon FSH and testosterone. Lithium also increased basal and TRH stimulated release of TSH and basal prolactin levels. Lithium was without effect upon prolactin responses to TRH. The results are discussed in relation to current information on the mechanism of lithium's action. The implications for neuroendocrine work on recovered patients taking lithium are also explored.

Adult↗
PubMed2003

An efficient conversion of (3R,3'R,6'R)-lutein to (3R,3'S,6'R)-lutein (3'-epilutein) and (3R,3'R)-zeaxanthin.

Two dietary carotenoids, (3R,3'R,6'R)-lutein (1) and (3R,3'R)-zeaxanthin (2), and their metabolite (3R,3'S,6'R)-lutein (3'-epilutein) (3) accumulate in human serum, milk, and ocular tissues. There is increasing evidence that compounds 1 and 2 play an important role in the prevention of age-related macular degeneration. Therefore, the availability of these carotenoids for metabolic studies and clinical trials is essential. Compound 1 is isolated from extracts of marigold flowers (Tagete erecta) and is commercially available, whereas 2 is only accessible by a lengthy total synthesis, and a viable method for synthesis of 3 has not yet been developed. This report describes an efficient conversion of technical grade 1 to 2 via 3. Acid-catalyzed epimerization of 1 yields an equimolar mixture of diastereomers 1 and 3. The mixture was separated by enzyme-mediated acylation with lipase AK from Pseudomonas fluorescens that preferentially esterified 3 and after alkaline hydrolysis yielded this carotenoid in 90% diastereomeric excess (de). Compound 3 was also separated from 1 in 56-88% de by solvent extraction and low-temperature crystallization, Soxhlet extraction, or supercritical fluid extraction. Base-catalyzed isomerization of 3 gave 2 in excellent yield, providing a convenient alternative to the total synthesis of this important dietary carotenoid.

Biotransformation↗
PubMed1986

Effects of parathyroidectomy in pregnant rats on the luteinizing hormone and follicle-stimulating hormone response to synthetic luteinizing hormone-releasing hormone in the infantile offspring.

Effects of parathyroidectomy (PTx) in the rat at the 5th day of gestation on the functional development of gonadotrophin secretion in the infantile offspring was examined. A single subcutaneous injection of 10 micrograms/kg of luteinizing hormone-releasing hormone (LHRH) induced a significant increase in serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) in control- and PTx-F1 male and female rats already at 3 days of age. The response in female rats was greater than in males at all ages examined. In the control- and PTx-F1 rats, age-related increase in the responsiveness to LHRH was observed in both sexes for LH but only in females for FSH. However, LH and FSH release by LHRH in the PTx-F1 female rats was significantly lower than that in control females at 14 and 22 days of age. In the PTx-F1 male rats, only FSH response to LHRH showed a tendency to decrease at 22 days of age. Serum calcium levels in 3-day-old PTx-F1 male and female rats were significantly lower than those in controls but only a slight decrease was observed in the PTx-F1 rats at other ages. The present results indicated that a low serum calcium environment during fetal life in the rat affects the functional development of pituitary responsiveness to LHRH, particularly in females.

Animals↗
PubMed1993

Effect of protein deficiency on luteinizing hormone releasing hormone (LHRH), gonadotropin releasing hormone associated peptide (GAP) and luteinizing hormone (LH) immunocytochemistry in the hypothalamus and pituitary gland of prepubertal ewes.

Growing female lambs were fed diets containing 14.2% (standard) or 8.1% (protein restricted) of proteins to determine their effects on puberty and luteinizing hormone releasing hormone (LHRH), gonadotropin hormone associated peptide (GAP), luteinizing hormone (LH) hormonal system. At the end of the experiment (30-34 weeks of age), hypothalamic LHRH, GAP and pituitary LH were analysed by immunocytochemical methods using specific antibodies. Plasma LH were determined by radioimmunoassay at 21 weeks of age. It was found that lowering of the dietary proteins content decreased the concentration of basal plasma LH significantly in lambs of 21 weeks of age. None of the sheep of this group reached sexual maturity at the same time as the animals of the standard group. However, immunoreactive (ir) LHRH neuronal system of protein restricted lambs was normally developed: Numerous irLHRH perikarya, dense network of axons and abundant material stored in the nerve terminals were well visualized in the typical sites of the preoptico-septal area, hypothalamus and the median eminence (ME). Gonadotropin associated peptide (GAP) of the LHRH precursor was present in the same populations of neurons that contained LHRH in the sheep brain. The proportion of pituitary LH-cells was three fold higher in pituitaries of the nutritionally restricted group. They displayed hypertrophy and very strong immunoreaction. These results show that protein deficiency in diets of growing female sheep delays their puberty but does not impair the synthesis and processing of LHRH in the brain neurons and synthesis of LH in pituitary cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗