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Ultrastructure and morphometry of testicular Leydig cells and the interstitial components correlated with testosterone in aging rats.

The ultrastructure of testicular interstitium in young and aged adult rats was analysed using morphometric methods, and the plasma testosterone concentration was measured. With increasing age there was an augmentation in the volume of collagen fibrils in the intercellular matrix and in blood vessels. During the aging process (approximately two years) the average volume of the Leydig cell decreased from 1364 microns 3 to 637 microns 3, but the number of Leydig cells in paired testes increased from 53 x 10(6) to 113 x 10(6). The absolute volume of smooth surfaced endoplasmic reticulum (SER) per Leydig cell amounted in aged rats to 78% of that in young adult rats. The total amount of SER in paired testes increased by 62% with aging. The present analysis suggests that the ability of SER to maintain peripheral testosterone concentration decreases with age. In young adult rats the absolute volume of peroxisomes per Leydig cell correlated significantly with the concentration of testosterone in blood and also with the absolute volume of SER per Leydig cell. These results combined with ultrastructural observations of close apposition of peroxisomes and SER suggest that peroxisomes have a role in testosterone secretion by Leydig cells.

Aging↗

Testicular control of defeminization in male pigs.

Female mating behavior, defined as expression of the immobilization response ("mating stance") in the presence of an intact male, was monitored in gonadectomized, hormone-treated female and male pigs to evaluate sexual dimorphism for this trait. When treated postpubertally with estradiol benzoate (EB), the relationship between dosage of EB and proportion of pigs that showed an immobilization response, as well as duration of this response, was similar in ovariectomized females and males castrated at 2 weeks of age (neonatally). Males castrated at 8 months of age (post-pubertally) showed little response to EB treatment. In males castrated at different ages from birth to 8 months, the proportion showing an immobilization response was less for males castrated at 6 months than observed in males castrated at birth or 2 months of age, and the duration of response to EB was shorter for males castrated at 4 months of age or later. When androgens were evaluated for their effectiveness, testosterone propionate (TP), at the dosages used, induced the immobilization response in all females and neonatally castrated males. Females did not show a response to dihydrotestosterone propionate treatment. An immobilization response was observed in some, but no all, postpubertally castrated males with high dosages of EB or TP; but the frequency of response did not increase with increasing dosage of TP greater than 250 micrograms/kg body weight. These observations indicate that female mating behavior in pigs is a sexually dimorphic trait and suggest that the sensitive period sexual differentiation of this trait in males is associated with increased testosterone secretion during pubertal development.

Aging↗

Smith-Lemli-Opitz syndrome: in vivo and in vitro study of testicular function in a prepubertal patient with ambiguous genitalia.

The pathogenesis of the development of ambiguous genitalia reported in some 46,XY patients with Smith-Lemli-Opitz syndrome is not understood. Presumably, it is related to the 7-dehydrocholesterol reductase deficiency present in these patients. In this study we have evaluated testicular function, both in vivo and in vitro, in a 46,XY patient with ambiguous genitalia, reared as a girl. The diagnosis was based on clinical features, low serum cholesterol and high serum 7-dehydrocholesterol levels. Serum hormone values, determined during the first month of age, showed normal basal testosterone (1.95 ng/ml), LH (0.91 U/l) and FSH (2.51 U/l). However, serum testosterone did not increase after hCG administration (1.98 ng/ml). On the other hand, the patient had a positive biological response to exogenous testosterone (decrease in sex hormone-binding globulin serum levels). She was orchidectomized at the age of 33 mo. Testicular cells were dispersed and maintained in culture for 6 d. These cells showed a very good capacity to secrete testosterone into the culture medium (X +/- SD, 26.1 +/- 11.7 vs. 4.36 +/- 1.70 pmol/10(6) cells/24 h in a control group of testicular cells prepared from testes collected at necropsy). The patient's cells failed to respond to LH stimulation (18.6 +/- 4.0 pmol/10(6) cells/24 h), although they did respond to other stimuli. It is concluded that the severe cholesterol deficiency of this patient did not impair the capacity of the testes to synthesize testosterone. However, the LH/hCG receptor or its subsequent message was activated neither in vivo nor in vitro. This finding suggests that the foetal testes might have failed to respond to placental hCG at the time of male external genital differentiation. This failure could have been responsible for the ambiguous genitalia present in this patient.

Cells, Cultured↗

Comparisons of the nuclear uptake of [3H]-testosterone and its metabolites by the brains of male and female macaque fetuses at 122 days of gestation.

Testosterone secreted by the testis of the macaque fetus is thought to influence certain aspects of the brain's subsequent development which may be responsible for the ontogeny of sexually dimorphic patterns of behavior. To compare the interactions between testosterone and the receptors for androgens and estrogens in brain cell nuclei in the two sexes, 7 intact female fetuses and 5 intact male fetuses were injected in utero at about 120 days of gestation with [3H]-testosterone (250 microCi i.v. or 500 microCi s.c.). One hour later, fetuses were delivered by cesarean section, and samples of brain and peripheral tissues were homogenized and separated into purified nuclear and supernatant fractions. Fractions were analyzed by high performance liquid chromatography to measure levels of [3H]-testosterone and its metabolites. Concentrations of radioactivity extracted from cell nuclei were significantly higher in the hypothalamus-preoptic area than in other brain areas (p less than 0.001); [3H]-estradiol represented 65.0 +/- 5.7% of this radioactivity and nuclear concentrations of this metabolite were 73% lower in males than in females (p less than 0.001). Nuclear concentrations of [3H]-testosterone in the pituitary gland (68.9 +/- 8.8% of extracted radioactivity) were 48% lower in males than in females (p less than 0.001). There was no evidence of a sex difference in the tissue uptake of radioactive steroids from blood, but in males, levels of endogenous plasma testosterone (599.8 +/- 208.2 ng/100 ml) were significantly higher than in females (37.7 +/- 28.5 ng/100 ml; p less than 0.01), and the specific activity of [3H]-testosterone in blood was consequently lower in males than in females.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Pituitary and testicular responses in sexually mature bulls after intravenous injections of graded doses of LH-releasing hormone.

The capacity of the anterior pituitary gland and testes in mature bulls (705 +/- 9 (S.E.M.) kg body wt, n = 4) to respond to graded doses of LH-releasing hormone (LHRH) was assessed relative to endogenous profiles of LH and testosterone secretion. Endogenous hormone profiles were determined by bleeding bulls at 20-min intervals for 12 h. Responses to LHRH were assessed on successive days after single intravenous injections of 1, 5, 10, 50 or 100 ng LHRH/kg body wt. Blood samples were taken at -40, -20, 0, 10, 20, 30, 40, 60 and 120 min relative to LHRH injection. During a 12-h bleed bulls showed spontaneous pulses of LH and testosterone which had peak amplitudes of 2.6 +/- 0.5 micrograms/l and 44.5 +/- 7.1 nmol/l respectively. Respective peak LH (micrograms/l) and testosterone (nmol/l) responses to LHRH were as follows: 1 ng LHRH (3.0 +/- 0.7; 47.3 +/- 4.1); 5 ng LHRH (8.0 +/- 1.2; 52.8 +/- 6.2); 10 ng LHRH (11.1 +/- 2.3; 57.7 +/- 9.1); 50 ng LHRH (19.2 +/- 2.8; 47.9 +/- 8.6); 100 ng LHRH (19.1 +/- 4.7; 43.9 +/- 6.4). A dose of 1 ng LHRH/kg produced LH and testosterone responses which were comparable in amplitude to spontaneous peaks in the respective hormone. There was a linear (y = 0.28 X + 5.72; r = 0.81) increase in the LH response to doses of LHRH between 1 and 50 ng/kg; corresponding testosterone responses showed no relationship with the dose of LHRH. The capacity of the anterior pituitary gland to release amounts of LH eight to ten times in excess of those secreted during spontaneous peaks suggests that (1) there exists a large releasable store of LH in the anterior pituitary gland and (2) hypothalamic LHRH is a limiting factor in gonadotrophin secretion. In contrast to LH release, the androgenic response of the testes to acute gonadotrophic stimulation is determined largely by prevailing steroidogenic activity.

Animals↗

Prenatal androgens time neuroendocrine puberty in the sheep: effect of testosterone dose.

In sheep, prenatal exposure to androgens during a critical period for sexual differentiation of the brain (30-90 days of gestation; 145 days is term) can advance the timing of puberty in females and prevent the preovulatory LH surge. The present study tests the hypothesis that in sheep, the timing of neuroendocrine sexual maturation is related to the amount of prenatal steroid exposure. In addition, we determined if different steroid requirements exist for sexual differentiation of the tonic and surge modes of gonadotropin secretion. Testosterone was administered weekly to three groups of pregnant ewes from days 30-90 of gestation at doses of 200, 80, or 32 mg/week. The resulting androgenized female lambs together with control males and females (n = 5-7/group) were gonadectomized at 3 weeks of age, and gonadal steroids were replaced with a SILASTIC brand estradiol-filled capsule. LH concentrations were measured from biweekly blood samples. Sustained increases in circulating LH were considered to reflect the initiation of neuroendocrine puberty. In male lambs, LH secretion started to increase at 8.3 +/- 0.9 weeks of age (mean +/- SEM). The two highest doses of prenatal androgen advanced the onset of neuroendocrine sexual maturation in females. In the 200 mg androgenized females, the pubertal LH rise (10.2 +/- 2.0 weeks) began about the same time as in males. In the 80 mg treatment group, LH concentrations increased at 16.2 +/- 1.5 weeks, which was later than in males, but well before that in normal females (27.1 +/- 0.7 weeks). For females treated with the lowest dose of androgen (32 mg), the pubertal LH increase (24.6 +/- 1.9 weeks) began about the same time as in normal females. To test the function of the LH surge system, LH was measured every 2 h for 60 h after an acute increase in circulating estradiol was produced by implanting additional estrogen capsules. All control females produced a surge in response to acute estradiol stimulation. LH surges did not occur in males, 200 mg androgenized females, or 80 mg androgenized females. Of six females from the 32 mg treatment group, two produced LH surges in response to the stimulatory feedback action of estradiol. We conclude that the greater the amount of prenatal testosterone, the earlier the initiation of the pubertal LH rise. Moreover, the finding that low doses of testosterone (32 mg/week) are capable of abolishing the LH surge without significantly advancing the timing of puberty supports our hypothesis that different steroid requirements exist for sexual differentiation of tonic and surge modes of LH secretion.

Aging↗

Inhibitory effect of plasma obtained from hypophysectomized and control women on the assay of bioactive luteinizing hormone.

The purpose of this study was to determine the effect of components of female plasma on the value of bioactive luteinizing hormone (LH), especially in the presence of low immunological LH value. Using both an immunoradiometric assay (IRMA) and rat Leydig cell bioassay, immunoreactive (I) and bioactive (B) LH were assessed in plasma collected from women during a gonadotrophin releasing hormone (GnRH) test performed on day 7 of a spontaneous cycle. Two modes of response to an acute administration of GnRH were defined: normal production of gonadotrophins (group I) and excessive secretion (group II) associated with a significant difference in the B/I-LH ratio between the two groups. The B/I-LH ratio did not vary with sampling time during the test in either group. The addition of LH-free plasma collected from hypophysectomized women caused a 30% decrease in testosterone production compared to control values (in the presence or absence of hLH standard). A partial restoration of testosterone production was observed if plasma was first treated with PEG 12%. The inhibitory factor(s) was also present in plasma from ovulatory women, even after treatment by an antibody against the entire LH molecule. The effect of normal (A) or low I-LH plasma (B) on testosterone production varied strongly according to the plasma volume added to the bioassay, as well as to plasma treatments. Diethylether treatment caused a 50% decrease in testosterone secretion for plasma B (but not for A) whereas a diminution of the steroidogenesis is observed after a PEG treatment of plasma A (but not for B), suggesting that different inhibitory factors are present in plasmas A and B. Therefore the LH bioactivity measured in the rat Leydig cell assay, in terms of testosterone output, seems to represent a balance between the LH molecule and the presence of inhibitory factors in the plasma.

Adult↗

Differentiation of the fetal gonad.

Gonadal differentiation may be divided into four stages: pregonadal, indifferent, primary sex differentiation, and secondary sex differentiation. Sertoli cells appear at 6-7 weeks and Leydig cells differentiate at 8 weeks, but in ovaries, primary sex differentiation occurs much later. Testosterone secretion peaks at 12-16 weeks causing male secondary sex development together with the appearance of anti-Müllerian hormone. Fetal testis is able to synthesize and secrete inhibins. Lower circulating luteinizing hormone (LH) and follicle stimulating hormone (FSH) levels in male than in female fetuses at midgestation suggest that the fetal pituitary is already responsive to the gonadal hormones. Placental human chorionic gonadotrophin may regulate testosterone synthesis at midgestation, and both LH and FSH are likely to have some regulatory effect on fetal gonads during the last third of gestation.

Female↗

Reproductive hormone secretion and spermatogenic function in thyroidectomized rams receiving graded doses of exogenous thyroxine.

This study aimed to obtain a better understanding of the relationship between circulating thyroxine (T4) concentrations and reproductive endocrine function in the ram. Mature Merino rams were thyroidectomized and supplemented with 0, 30, 100 and 300% of normal T4 for 10 weeks. Thyroidectomy had no apparent effect on spermatogenic function but interfered with sperm maturation, the latter being returned to normal by 30% T4 replacement. Circulating testosterone levels were reduced by thyroidectomy and restored to control levels by 30% T4; when T4 levels were supranormal (300%), circulating testosterone levels were again reduced. The lowered circulating testosterone levels in thyroidectomized rams occurred as a result of suppressed testosterone secretion from the testis, observed under basal conditions and also following LH-releasing hormone (LHRH) and human chorionic gonadotrophin injection. In thyroidectomized rams, sex hormone binding globulin (SHBG) levels were depressed without changes in testosterone clearance rate (TCR), while in rams with supranormal T4 levels, TCR was increased without changes in SHBG levels. Subnormal levels of T4 also restored to normal the reduced LH pulse frequency in thyroidectomized rams. Reduced LH pulse frequency, together with diminished LH release following LHRH injection in thyroidectomized rams, suggested effects of T4 at the hypothalamo-pituitary axis. The present study demonstrates that complete lack of thyroid hormones suppresses normal reproductive endocrine function in the ram, but that this can be restored to normal by 30% T4 replacement. The results support the theory that T4 plays a permissive rather than a regulatory role in reproductive function in males.

Animals↗

Testicular androgens in prostate cancer patients treated with a luteinizing hormone releasing hormone agonist.

Luteinizing hormone releasing hormone agonists have been shown to reduce the levels of androgens in the peripheral circulation and to reduce prostate volume. The objective of this study was to quantify testicular function in patients with metastatic carcinoma of the prostate treated with a luteinizing hormone releasing hormone agonist, leuprolide, by analysis of spermatic vein blood for testosterone and androstenedione, and by determination of the maximum velocity of the 17 beta-hydroxysteroid oxidoreductase enzyme in testicular tissue in vitro. A chemical analysis of the spermatic vein blood of 19 patients with a median age of 78 years revealed the presence of significantly high levels of testosterone and androstenedione, 20.7 +/- 1.9 micrograms % and 6.7 +/- 0.7 micrograms %, respectively. These androgens could not be detected in patients treated with leuprolide before orchiectomy. Patients treated with leuprolide for several months followed by a period of no treatment before orchiectomy secreted testosterone and androstenedione levels comparable to the control group. The maximum velocity of the 17 beta-hydroxysteroid oxidoreductase enzyme in vitro in the testes of the leuprolide treated patients was significantly inhibited. Enzyme activity returned to normal levels when leuprolide treatment was followed by a recovery period of no treatment before orchiectomy.

17-Hydroxysteroid Dehydrogenases↗

Importance of perinatal testosterone in sexual differentiation in the male rat.

Testosterone secretion in the male rat was high during the late fetal and immediate postnatal periods. It then showed a rapid decrease 3h after birth and remained low until puberty. Male rats from mothers given daily injections of an antibody to testosterone during the week before delivery displayed an LH peak when they were adult, orchidectomized and implanted with oestradiol. However, the amplitude of the peak was far smaller than in female rats from the same mothers treated in the same manner. Thus, the critical period during which testosterone triggers hypothalamic sexual differentiation is very close to birth, possibly starting at the end of the fetal period.

Animals↗

Leydig cell tumor of the testis: analysis of testosterone production and secretion by three-dimensional histoculture.

We treated an 11-year-old boy with a testicular Leydig cell tumor. We analyzed the testosterone production of this tumor by immunolocalization of steroidogenic enzymes and in vitro three-dimensional histoculture. Spermatic venous blood from the tumor bearing testis had noticeably high concentrations of testosterone and androstenedione. The tumor had the characteristic ultrastructural features of steroid producing cells and was immunoreactive for P450scc (side chain cleavage), 3 beta HSD (hydroxysteroid dehydrogenase) and P450c17 (17 alpha-hydroxylase). Three-dimensional collagengel-supported histoculture demonstrated that the tumor tissue in the culture maintained its histologic architecture, expression of steroidogenic enzymes, and secretion of testosterone into the medium for up to 7 days in culture. Histoculture preserved in vitro testosterone production in this case of testicular Leydig cell tumor.

3-Hydroxysteroid Dehydrogenases↗

Histogenesis, cytodifferentiation, and its subcellular steroidogenic sites in the virilizing ovarian Leydig cell tumor: light microscopic dry-mounting radioautography for [3H]cholesterol and electron microscopic cytochemistry for 3 beta-hydroxysteroid dehydrogenase activity.

A case of a virilizing ovarian Leydig cell tumor in a 38-year-old woman with a marked elevated plasma testosterone level was investigated using light microscopic dry-mounting radioautography and electron microscopic cytochemistry. Following a total abdominal hysterectomy and bilateral salpingo-oophorectomy, the plasma testosterone level decreased abruptly. Light microscopic dry-mounting radioautography for [3H]cholesterol showed silver grains localized mainly over the cytoplasm of the neoplastic Leydig cells which were of three different cell types: fibroblast-like cells, Leydig cells (steroid-secreting cells), and transitional cells (partially or incompletely differentiated Leydig cells). Reaction products for 3 beta-hydroxysteroid dehydrogenase activity were localized on the tubular or lamellar cristae and inner membranes of the mitochondria, and on the membranes of smooth endoplasmic reticulum in the transitional cell as well as in the Leydig cell. From these observations, it is suggested that the Leydig cell tumor is derived from the fibroblast-like cell and from the transitional cell, morphologically falling between the fibroblast-like cell and the Leydig cell, has fine structural evidence of steroidogenic activity, and has an ability to secrete testosterone.

3-Hydroxysteroid Dehydrogenases↗

Rapid down-regulation of testicular androgen biosynthesis at increased environmental temperature is due to cytochrome P450c17 (CYP17) thermolability in Leydig cells, but not in endoplasmic reticulum membranes.

To identify possible molecular targets in moderate heat-induced, short-term derangements of rat testicular endocrine function, rates of androgen and precursor biosynthesis and key enzyme concentrations were compared at 38 degrees C (normal body core temperature) and 31 degrees C (normal scrotal temperature) in three in-vitro models of decreasing complexity and increasing specificity. In purified Leydig cells and similarly in decapsulated testes, gross testosterone secretion was by 20% higher at 38 degrees C under basal conditions and during the initial phase of stimulation with hCG or cAMP; longer (> 1 hour) exposure to the elevated temperature resulted in a marked decrease (52% after 3 hours) of testosterone response to hCG or cAMP as compared to the corresponding rates at 31 degrees C. This phenomenon was neither due to the development of hormone resistance at the receptor level nor to restricted cholesterol supply and turnover nor to increased testosterone accumulation. Whereas mitochondrial CYP11A (cytochrome P450cscc: cholesterol monooxygenase) was absolutely temperature-insensitive in all systems tested, CYP17 (cytochrome P450c17: steroid-17 alpha-monooxygenase/C17, 20-aldolase) in the smooth endoplasmic reticulum responded with a 57% loss in whole testes and 39% loss in purified Leydig cells upon a 3-hour temperature elevation from 31 degrees C to 38 degrees C. In contrast, CYP17 was stable (4% loss) when tested directly in microsomal membranes. It is concluded that CYP17, but not CYP11A, is very sensitive towards even moderate elevation of environmental temperature, and that this apparent lability is not an intrinsic property of the enzyme protein but rather mediated by heat-activated intracellular factors.

Androgens↗

Neonatal phenobarbital-induced persistent alterations in plasma testosterone profiles and testicular function.

Daily sc injections of phenobarbital at anticonvulsant therapeutic doses for the rat (40 mg/kg) for the first 7 days of life resulted in below normal levels of serum testosterone from around birth to before puberty, normal levels during puberty and above normal levels of the androgen after puberty and in adulthood. Cluster analysis of the plasma testosterone secretory profiles obtained at 15-min intervals from phenobarbital-treated rats at 65 and 165 days of age revealed a significant increase in both the peak amplitudes and their durations resulting in a 100% increase in the amount of hormone secreted during the peak periods. In general, most of the rats (control and experimental) secreted testosterone as two large peaks, each 3 to 4 hr in duration, during the 10-hr lights-on collection period. In addition to permanently disrupting the ultradian profiles of plasma testosterone, neonatal exposure to the barbiturate altered testicular responsiveness to steroidogenic regulatory agents. That is, neonatal exposure to phenobarbital enhanced the responsiveness to exogenous hCG as measured by an above-normal increase in testosterone concentration. Moreover, phenobarbital-induced reductions in serum testosterone levels were delayed in adult rats neonatally exposed to the barbiturate. Whereas a single challenge dose of phenobarbital (1 or 10 mg/kg) reduced serum testosterone concentrations in control animals by almost 80% within 3 hr, a decline in serum androgen levels in the neonatally phenobarbital exposed males was not observed until 12 hr after the challenge dose. These results indicate that postpartum exposure to therapeutic levels of phenobarbital can permanently disrupt testosterone secretory profiles and alter pathways regulating testicular steroidogenesis.

Aging↗

Leydig-cell function in children after direct testicular irradiation for acute lymphoblastic leukemia.

To assess the effect of testicular irradiation on testicular endocrine function, we studied 12 boys with acute lymphoblastic leukemia who had been treated with direct testicular irradiation 10 months to 8 1/2 years earlier. Insufficient Leydig-cell function, manifested by a low response of plasma testosterone to chorionic gonadotropin or an increased basal level of plasma luteinizing hormone (or both), was observed in 10 patients, 7 of whom were pubertal. Two of these patients had a compensated testicular endocrine insufficiency with only high plasma concentrations of luteinizing hormone. Testosterone secretion was severely impaired in three pubertal boys studied more than four years after testicular irradiation. A diminished testicular volume indicating tubular atrophy was found in all pubertal patients, including three who had not received cyclophosphamide or cytarabine. These data indicate that testosterone insufficiency is a frequent complication of testicular irradiation, although some patients continue to have Leydig-cell activity for several years after therapy.

Adolescent↗

Experimental studies on the annual cycles of thyroid and adrenocortical functions in relation to the reproductive cycle of drakes.

The annual variations in the basal plasma contents of testosterone, thyroxine and corticosterone have been measured in Peking drakes living outdoors, in Southern France. 10 The plasma testosterone titer underwent a more than 20-fold increase during the vernal reproductive period (March-April). In early June the circulating testosterone fell to near autumnal values, and the testosterone MCR was augmented. These were the first manifestations of the cessation of the vernal reproductive period. 20 The plasma thyroxine levels were minimal in autumn, moderately augmented (40%) in winter (January-March), but exhibited a 3-fold increase in early June. The resulting steep (13-fold) increase of the plasma thyroxine/testosterone ratio preceded the onset of the post-nuptial moult. 30 Modifications of testosterone secretion and clearance rate similar to those occurring in June were initiated in spring by i.m. injections of thyroxine at a dosage (1 mg/d) that induced June-July thyroxine plasma levels. On the other hand, an experimentally induced steep decrease of testosterone (castration) induced enhanced plasma thyroxine concentrations similar to the June values, while an induced (10 mg/d testosterone i.m.) hypertestosteronemia corresponding to the reproductive period depressed the plasma thyroxine levels. Strong reciprocal negative interactions between testis and thyroid might therefore afford a partial explanation of the peculiar thyroxine/testosterone imbalance that occurred in June immediately prior to the moult. 40 Cold-exposed "short-day" (December) ducks exhibited a marked increase in plasma thyroxine levels, while exposure of December ducks to "long days" (18L-6D) at 25 degrees C depressed the thyroxine titers. The inhibitory effect of "long days" on the blood level of thyroxine was further evident in castrated ducks. Exposure of "short day" ducks (December) to a combined treatment by "long days" (18L-6D) and cold (4 degrees C) produced an endocrine picture similar to the January-March pattern, i.e. highly increased testosterone plasma levels, but unaffected testosterone MCR, together with a moderate increase in plasma thyroxine concentration. 50 Corticosterone plasma concentrations increased during the reproductive season, as a result of a seasonally augmented binding-capacity of the CBG. Exogenous testosterone (10 mg/d) which induced spring-like circulating levels of male hormones, caused a similar increase in CBG-bound and total corticosterone levels. 60 In June the MCR of both corticosterone and aldosterone were elevated (as was the testosterone MCR). Similarly enhanced MCR of both corticosteroids were brought on in spring by an exogenous thyroxine treatment, leading to a June-like state of hyperthyroxinemia.

Adrenal Cortex↗

Active immunization of prepubertal boars against testosterone: testicular and endocrine responses at 14 months of age.

Thirteen crossbred boars were immunized at 1 mo of age against either testosterone-3-oxime-equine serum albumin (treated boars) or equine serum albumin (control boars) to test the hypothesis that active immunization against testosterone stimulates testicular growth and development in the prepubertal boar. All boars were injected with the appropriate antigen at 2, 3, 4, 5 and 6 mo of age and were slaughtered at 14 mo of age. Active immunization against testosterone resulted in an increase (P less than .05) in tritiated-testosterone binding by plasma within 60 d after the primary immunization; the degree of binding decreased by 6 mo but remained elevated (P less than .05) relative to controls through 12 mo of age. There was no effect of treatment on body weights through 12 mo of age. Concentrations of testosterone in plasma were higher (P less than .05) in testosterone-immunized boars than in controls; this increase was likely due to antibody binding rather than increased testosterone secretion because (1) concentrations of androgen in testicular parenchyma at slaughter were not altered by treatment and (2) plasma concentrations of estrogens were generally not affected by treatment. Concentrations of luteinizing hormone (LH) and follicle stimulating hormone (FSH) were markedly suppressed in testosterone-immunized boars during the time when concentrations of these gonadotropins were high in control boars (greater than 3 mo of age). In spite of suppression of average LH and FSH concentrations, testicular weights, daily sperm production rates and seminal characteristics were similar for the two groups of boars at slaughter. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗