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PubMedDate not supplied

Effect of PCB 126 and PCB 153 on incidence of apoptosis in cultured theca and granulosa cells collected from small, medium and large preovulatory follicles.

The aim of the presented study was to evaluate the effects of PCB 126 and PCB 153 on granulosa and theca cell apoptosis. Granulosa and theca cells were collected from small, medium, and large preovulatory porcine follicles and cultured as monolayers. Cells were initially cultured for 24 h to allow attachment to the plates. Media were changed and 100 pg/ml PCB 126 or 100 ng/ml PCB 153 were added. After 48 h, granulosa and theca cells were fixed for assessment of the number of apoptotic cells utilizing a Hoechst staining technique or frozen for measurement of caspase-3 activity. Media were collected for testosterone concentration analysis from theca cell cultures or estradiol from granulosa cell cultures. Neither PCB 153 nor PCB 126 had an effect on testosterone secretion by theca cells collected from small and medium size follicles, while both PCBs decreased testosterone secretion by large follicles. The decrease in testosterone secretion by large follicles under the influence of both PCBs was paralleled by a suppression of caspase-3 activity and a decreased incidence of apoptotic bodies. Neither of the PCBs had an effect on estradiol secretion by granulosa cells collected from small and medium size follicles, while both PCBs increased estradiol in granulosa cells collected from large follicles. PCB-associated increased estradiol secretion by granulosa cells collected from large follicles was accompanied by suppression of caspase-3 activity and a decreased incidence of apoptotic bodies. In conclusion, we have presented evidence that in preovulatory follicles PCBs inhibit both theca and granulosa cells apoptosis. Therefore, an exposure to PCBs may cause alterations in the pattern of terminal differentiation of follicles and attenuate spontaneous elimination of atretic follicles.

Animals↗
PubMed2026

Study on the mechanism of SW inhibiting testosterone synthesis in mouse Leydig cells.

BACKGROUND: Swainsonine (SW), the main toxic component of locoweed, can cause livestock poisoning and reproductive damage in male animals; however, the mechanism by which it affects testosterone secretion remains unclear. METHODS: Ten-week-old male C57BL/6 mice were orally administered SW at doses of 0, 0.05, and 0.25 mg/(kg·d) for 28 days. TM3 mouse Leydig cells were treated with SW at concentrations of 0, 1, and 10 nM for 24 h. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was performed on RNA-seq data from mouse testicular tissues to identify differentially enriched pathways between the control and SW-treated groups. Testosterone secretion levels were measured using an enzyme-linked immunosorbent assay (ELISA). The mRNA expression levels of steroidogenesis-related genes (StAR, Cyp11a1, Hsd3b2, and Hsd17b3) were detected by qPCR, while the expression of the steroidogenic acute regulatory (STAR) protein was detected by western blotting. AutoDock Vina molecular docking was used to predict the binding affinity between SW and the STAR protein. RESULTS: KEGG analysis revealed a significant enrichment of pathways related to steroid synthesis. In both the mouse model and TM3 cells, SW significantly inhibited testosterone secretion, downregulated the mRNA expression of StAR, Cyp11a1, Hsd3b2, and Hsd17b3, and reduced the protein expression of STAR. Molecular docking analysis revealed multiple potential hydrogen-bond interaction sites between SW and STAR. CONCLUSION: SW downregulates the expression of steroidogenesis-related genes and STAR protein, thereby suppressing testosterone secretion in male mice and TM3 cells.

Swainsonine↗
PubMedDate not supplied

Chronic propranolol treatment causes desensitization of the steroidogenic response in testicular interstitial cells but does not alter protein kinase C.

We investigated effects of chronic propranolol treatment on the secretory response of rat testicular interstitial cells (testosterone secretion) to subsequent in vitro stimulation with activators of protein kinase-C (PK-C) (L-propranolol, phorbol 12, 13-dibutyrate (PDBu), LHRH) or activators of protein kinase A (PK-A), (hCG or dibutyryl cAMP (dbcAMP)). We determined [3H]PDBu binding and PK-C activity in these cells. Treatment of rats with propranolol (Inderal 500 mg/L of water for 5 weeks) reduced by 48%, 50% and 29% the L-propranolol-, LHRH- or PDBu-induced testosterone secretion, respectively, when compared to cells from controls. This desensitization in testosterone secretion in vitro was also present when the testicular interstitial cells were stimulated with hCG or dbcAMP (secretion decreased by 65%/57%, respectively, when compared to cells from control rats). Challenging the cells originated from rats that received propranolol chronically with the addition in vitro of propranolol resulted in an additional reduction of the hCG/dbcAMP-stimulated testosterone secretion. Chronic propranolol-induced desensitization was not associated with a loss in [3H]PDBu binding or a decrease in PK-C activity. Chronic propranolol-induced desensitization can be uncoupled from down-regulation of protein kinase C. The effector responsible for the desensitization could be distal to the protein kinase C and protein kinase A.

Animals↗
PubMed1988

Effect of long term deprivation of luteinizing hormone on Leydig cell volume, Leydig cell number, and steroidogenic capacity of the rat testis.

Leydig cells atrophy, losing cytoplasmic volume and the capacity for testosterone secretion, within 1-2 weeks of LH deprivation. We investigated the effects of long term (0-16 weeks) LH deprivation on the volume of an average Leydig cell, the volume of Leydig cells per testis, the number of Leydig cells per testis, and testosterone secretion by in vitro perfused testes. Endogenous LH was suppressed in adult rats by testosterone/estradiol-filled (TE) Silastic implants. The presence of Leydig cells in testes was verified by 1) morphological examination using light and electron microscopy, 2) histochemical localization of 3 beta-hydroxysteroid dehydrogenase activity (3 beta HSD), and 3) conversion of pregnenolone to progesterone by in vitro perfused testes. Marked quantitative differences existed in Leydig cell morphology among control and treated rats. The volume of an average Leydig cell and the total volume of Leydig cells per testis decreased (P less than 0.01) rapidly and progressively after TE implantation. At 16 weeks, the average Leydig cell lost 90% of its cytoplasmic volume and 65% of its nuclear volume. Analysis of variance failed to detect a significant decline in Leydig cell number per testis, despite a 16% reduction from the value in control rats (22.2 +/- 1.5 x 10(6)) in rats treated for 16 weeks (18.7 +/- 1.5 x 10(6)). After TE implantation, LH-stimulated testosterone secretion by in vitro perfused testes diminished (P less than 0.01) rapidly to 5% of the control values at 1 week and less than 0.3% of the control value from 4-16 weeks. In contrast, 25% of 3 beta HSD activity was retained (P less than 0.01 vs. controls) at 16 weeks, based on the rate of pregnenolone conversion to progesterone. Moreover, testes of treated rats secreted progesterone at a rate twice that of controls, when the steroid secretion rates were expressed per volume of Leydig cell cytoplasm. Loss of the testosterone-secreting capacity of testes after LH withdrawal was associated with a loss in the volume, but not a significant loss in the number, of Leydig cells. Thus, LH was required to maintain the differentiated structure and function of Leydig cells, but was not required to maintain the overwhelming majority of Leydig cells in the adult rat testis through 16 weeks. Moreover, at least one steroidogenic enzyme, 3 beta HSD, was retained by Leydig cells after long term LH deprivation.

3-Hydroxysteroid Dehydrogenases↗
PubMed1993

The role of tumor necrosis factor-alpha in the regulation of mouse Leydig cell steroidogenesis.

Tumor necrosis factor-alpha (TNF alpha), a cytokine secreted by activated macrophages, has been shown to modulate Leydig cell steroidogenesis. The present study examined the regulation of mouse Leydig cell function by TNF alpha at the molecular level. The effects of TNF alpha on both basal and 8-Br-cAMP-stimulated testosterone production, as well as cholesterol side-chain cleavage enzyme (P450scc) and 17 alpha-hydroxylase/C17,20 lyase (P450c17), were investigated. Treatment of Leydig cells with 0.1, 1.0, and 10.0 ng/ml TNF alpha inhibited basal testosterone secretion by 20 +/- 5.0%, 61.1 +/- 6.6%, and 60.7 +/- 5.8% of control, respectively, but had no effects on basal P450scc messenger RNA (mRNA) or protein levels. Treatment of Leydig cells with 8-Br-cAMP caused a 150.7 +/- 32.9-fold increase in testosterone production and marked stimulation of P450scc and P450c17 mRNA and protein accumulation. TNF alpha caused a significant and dose-dependent inhibition of 8-Br-cAMP-stimulated testosterone secretion by 35.9 +/- 9.9%, 90.9 +/- 1.7%, and 96.9 +/- 1.4% with 0.1, 1.0, and 10.0 ng/ml TNF alpha, respectively. TNF alpha also caused a decrease in P450scc and P450c17 mRNA and protein. Treatment with 0.1, 1.0, and 10.0 ng/ml TNF alpha decreased 8-Br-cAMP-stimulated P450scc mRNA by 11.5 +/- 6.9%, 29.3 +/- 2.7%, and 59.2 +/- 8.7%, and decreased 8-Br-cAMP-induced P450c17 mRNA 41.9 +/- 13.5%, 95.7 +/- 2.3%, and 98.5 +/- 1.2%, respectively. The inhibitory effects of TNF alpha on 8-Br-cAMP-stimulated P450 enzyme protein accumulation were also dose dependent, 35.6 +/- 11.4%, 52.9 +/- 14.1%, and 56.0 +/- 7.9% inhibition of P450scc protein levels, and 65.8 +/- 9.4%, 95.5 +/- 1.9%, and 96.9 +/- 2.1% suppression on P450c17 protein levels were observed with 0.1, 1.0, and 10.0 ng/ml TNF alpha, respectively. The inhibitory effect of TNF alpha on 8-Br-cAMP-induced P450c17 mRNA expression was reversible. Within 48 h after the removal of TNF alpha from culture, P450c17 mRNA was restored to 80.6 +/- 3.1% of the level in cultures treated with 8-Br-cAMP alone for 4 days. TNF alpha-mediated inhibition of 8-Br-cAMP-stimulated testosterone secretion from Leydig cells was also reversible. In addition, no significant cell mortality was noted in TNF alpha-treated cells. These data demonstrate that TNF alpha inhibits both basal and 8-Br-cAMP-stimulated testosterone secretion from Leydig cells in a dose-dependent manner.(ABSTRACT TRUNCATED AT 400 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1994

Effects of single and repeated administration of prostaglandin F2 alpha on secretion of testosterone by male rats.

The effects of single and repeated administration of prostaglandin (PG) F2 alpha on the secretion of testosterone and the effect of PGF2 alpha on the action of human chorionic gonadotropin (hCG) were investigated in adult male rats. The concentrations of plasma and testicular testosterone followed by a single injection of 100 micrograms of PGF2 alpha into each testis were similar to controls given a single injection of 0.05 ml of vehicle into one testis. When 1 or 10 IU of hCG were injected into the jugular vein simultaneously with the intratesticular injection of PGF2 alpha, concentrations of testosterone increased in response to dose; again, the effect was similar in controls. When 100 micrograms of PGF2 alpha was injected into each testis daily for 5 days, plasma testosterone concentration decreased below that in the controls, but the LH concentration was unchanged. When 1 or 10 IU of hCG were injected into the jugular vein the day after the fifth injection of PGF2 alpha, concentrations of plasma and testicular testosterone increased in response to dose; the effect was similar in controls. These results indicate that repeated stimulation by PGF2 alpha directly inhibits testosterone production in the rat testis without mediation by LH, and that PGF2 alpha does not affect the action of an LH-like substance.

Animals↗
PubMed1991

Sleep EEG and nocturnal secretion of testosterone and cortisol in patients with major endogenous depression during acute phase and after remission.

Sleep EEG and the nocturnal secretion of cortisol and testosterone in 12 male patients (mean age 46.4 +/- 11.26 years) with major endogenous depression were investigated concomitantly during acute depression, before treatment and after recovery and drug cessation. Testosterone concentration increased after remission, while cortisol secretion decreased. Sleep EEG disturbances remained unchanged in remitted patients. The data suggest that a blunted testosterone and an elevated cortisol secretion are state markers of acute depression, which normalize independently from sleep structure. An interaction between the hypothalamic-pituitary-gonadal axis and the limbic-hypothalamic-pituitary-adrenocortical axis appears likely.

Adult↗
PubMed1983

Biphasic effect of gonadotropin-releasing hormone and its agonist analog (HOE766) on in vitro testosterone production by purified rat Leydig cells.

GnRH and GnRH agonists have stimulatory and inhibitory effects on testicular testosterone secretion both in vivo and in vitro. To determine whether they are exerted directly on the Leydig cells and to explore the temporal relationships, we examined the effects of acute (3 h) and chronic (24-72 h) exposure of purified (greater than or equal to 80%) rat Leydig cells to GnRH and its agonist analog HOE766 (D-Ser-t-BU6,des-Gly-NH2 10LHRH ethylamide; Hoechst, Frankfurt, Germany) on testosterone production. GnRH and HOE766 enhanced basal testosterone secretion by freshly isolated or cultured Leydig cells. HOE766 was at least 100 times more potent than GnRH. However, exposure of Leydig cells to HOE766 for 24 h or longer lead to a significant reduction in hCG responsiveness without altering basal testosterone secretion. Both the stimulatory and inhibitory effects were dose related, with a maximal response elicited by 10(-9) M HOE766. HOE766 reduced Leydig cell sensitivity to hCG (ED50) stimulation, but did not alter the slope of the dose-response curves. Thus, GnRH and its agonist appear to have a dual and biphasic effect on the Leydig cells. Acute exposure stimulates basal testosterone secretion (and occasionally the hCG response), whereas chronic exposure decreases the response to hCG stimulation. These data provide additional evidence that GnRH has a direct effect on Leydig cell steroidogenesis.

Animals↗
PubMed2006

Innervation and serotoninergic receptors of the testis interact with local action of interleukin-1beta on steroidogenesis.

Testosterone secretion by Leydig cells is affected by interleukin-1beta (IL-1beta). The aim of the present study was to investigate whether partial denervation of the testis or local administration of a serotonin (5-HT) receptor antagonist could alter the changes in testicular steoidogenesis induced by IL-1beta. Intratesticular administration of IL-1beta was combined with vasectomy or local injection of ketanserin (5-HT type 2 receptor antagonist) in immature hemicastrated rats and the effect of the interventions on testicular steroidogenesis was studied. One day after treatment with local injection of IL-1beta induced a significant rise in testosterone secretion that could be prevented by vasectomy (that also means transection of the inferior spermatic nerve). In a model in which neither IL-1beta nor ketanserin interfered with steroidogenesis, administration of the receptor antagonist just prior to IL-1beta treatment significantly reduced testosterone secretion. Data indicate interaction between testicular nerves and IL-1beta action and interaction between testicular 5-HT2 receptors and local effect of IL-1beta on testosterone secretion.

Analysis of Variance↗
PubMed1986

Testosterone and estradiol are co-secreted episodically by the human testis.

In spite of a striking pulsatile pattern of luteinizing hormone (LH) secretion, testosterone (T) fluctuations in peripheral blood in normal adult men are irregular and of low amplitude. To determine whether T secretion by the human testis is episodic, T was measured in blood samples drawn at 15-min intervals for 4 h through a catheter placed in the testicular vein of six men with varicocele-associated infertility. Estradiol (E2) concentrations were also determined in each sample. Each subject released testosterone in well-defined pulses. Gonadal vein T levels ranged from 1 to 1,540 ng/ml. Mean (+/- SE) pulse amplitude was 176 +/- 42 ng/ml, with a frequency of 4.0 +/- 0.3 pulses per 4 h. Testicular vein E2 levels ranged from 0.01 to 6.8 ng/ml. E2 secretory episodes were generally coincident with T pulses, and their amplitudes were highly positively correlated (r = 0.90, P less than 0.01). These results indicate that T secretion by the adult human testis is pulsatile, and suggest a functional relationship between intermittent LH secretion and normal testicular steroidogenesis in men. The failure to appreciate these fluctuations as hormone pulses in peripheral blood may relate to their absolute amplitude and frequency. The concordance between E2 and T pulses suggests that the Leydig cell, under LH control, is the source of most of the E2 secreted by the adult human testis.

Adult↗
PubMed1996

Effect of intratesticular administration of somatostatin on testicular function in immature and adult rats.

Somatostatin has been demonstrated in the testis. In the present investigations the effect of intratesticular injection of somatostatin on serum testosterone level and in vitro basal testosterone secretion of the testis was studied in immature and adult rats. Intratesticular injection of somatostatin in adult rats with two testes in situ decreased serum testosterone concentration and basal testosterone secretion in vitro. Similar treatment in immature animals had no effect on the parameters studied. In immature hemicastrates, however, local administration of the peptide induced a significant rise both in basal testosterone secretion in vitro and serum testosterone level, and resulted in an increase in testicular weight. In adult hemicastrates the peptide did not influence testicular functions. These results indicate that somatostatin might play a modulatory role in testicular steroidogenesis. The data also suggest that the effect of somatostatin is age-dependent, and that hemicastration might modify local action of the peptide.

Aging↗
PubMed2004

Augmentation of growth hormone secretion after testosterone treatment in boys with constitutional delay of growth and adolescence: evidence against an increase in hypothalamic secretion of growth hormone-releasing hormone.

The increase in pituitary GH secretion that occurs during mid-late puberty in boys follows an increase in circulating testosterone (T) concentration; the direct mechanism by which this occurs is unknown. We hypothesized that T increases GH secretion during puberty by augmenting hypothalamic output of GHRH. Using constant infusions of a GHRH antagonist, we tested this hypothesis in six early pubertal boys with constitutional delay of growth and adolescence who had a mean chronological age of 14.0 +/- 0.3 yr and mean bone age of 11.4 +/- 0.2 yr. Blood samples were obtained from subjects every 15 min for 24 h during the overnight infusion of normal saline (2000-0600 h) and again during the overnight infusion of GHRH antagonist (0.33 microg/kg/h) the following night. Subjects then received transdermal T (5-mg patch) for 12 h nightly and were studied again after 4 wk of treatment. Serum samples were assayed for GH and total ghrelin; the percent suppression of GH during GHRH antagonist infusion was calculated. Morning serum T rose from 0.44 +/- 0.09 to 4.43 +/- 0.74 microg/liter (P = 0.005). T treatment was associated with a 92.6% increase in mean nocturnal GH secretion area under the curve (830 +/- 177 to 1599 +/- 340 microg/24 h.liter). Infusion of GHRH-antagonist suppressed mean nocturnal GH area under the curve by 29.1% before T treatment (830 +/- 177 to 621 +/- 168 microg/24 h.liter), and by 29.4% after T treatment (1599 +/- 340 to 1182 +/- 249 microg/24 h.liter; P = 0.99). Somatotroph sensitivity to GHRH was tested with 0.1- and 1.0-microg/kg doses of GHRH-44 iv; GH response did not change with regard to T treatment. The mean 24-h concentration of total ghrelin was unchanged with regard to T treatment. In summary, nightly transdermal T administration in six boys with constitutional delay of growth and adolescence increased GH output almost 2-fold, whereas the degree of GH suppressibility by GHRH antagonist remained unchanged. We conclude that the T-associated augmentation of GH secretion during early puberty in boys is unlikely to involve an absolute increase in hypothalamic GHRH output.

Adolescent↗
PubMed1993

[The effect of long-term prazosin treatment on plasma follitropin (FSH), lutropin (LH), prolactin, estradiol and testosterone concentration in male patients with essential hypertension].

UNLABELLED: The influence of prazosin treatment for 12 months on basal and LH-RH stimulated FSH, LH, estradiol and testosterone secretion and basal and chlorpromazine stimulated prolactin secretion was estimated in 15 male patients with essential hypertension. Male hypertensive patients were characterized by significantly elevated FSH and reduced testosterone secretion as compared with controls. In contrast, plasma LH, prolactin and estradiol concentrations were similar in both examined groups. After 12 months of prazosin treatment basal and stimulated LH and prolactin secretion significantly decreased while estradiol secretion significantly increased. Prazosin treatment for 12 months did not influence significantly LH and testosterone secretion. CONCLUSIONS: 1. Data presented in this study suggest the presence of abnormal function of the pituitary--gonadal axis in male patients with essential hypertension. 2. Long-term prazosin treatment shows an inhibitory effect on FSH and prolactin secretion but stimulatory one on estrogens secretion in male hypertensive patients.

Adult↗
PubMedDate not supplied

Effect of modulating endogenous prolactin secretion on testosterone production in the adult male bonnet monkey (Macaca radiata).

Adult male bonnet monkeys maintained under regulated light: dark conditions exhibit a nycthemeral surge of testosterone. The present study attempts to determine the effect of administration of drugs that modulate prolactin levels like ergobromocriptine (EBC) and chlorpromazine (CPZ) on testosterone production. The injection of EBC, a known inhibitor of prolactin secretion, could abolish nocturnal testosterone surge irrespective of the drug being given at 8.00 or 17.00 h. Testosterone surge could likewise be inhibited by treating animals with CPZ, a potent stimulator of prolactin secretion. This suggests that alteration in endogenous prolactin level from the normal effects nycthemeral surges of testosterone. The in vivo responsiveness of the testes of monkeys injected either CPZ oder EBC to exogenous LH or LHRH stimulation was tested. While LH could completely override the CPZ induced inhibition in testosterone production it could only partially reverse the EBC effect.

Animals↗
PubMed2006

[Isolation, cultivation, identification and functional study of fetal mice Leydig cells in vitro].

OBJECTIVE: To explore the methods of isolation, cultivation, purification, identification of the fetal mice testis Leydig cell and to observe its biological characteristics in vitro. METHODS: Leydig cells were isolated by 0.03% collagenase (type I) from fetal mice testis and cultured in DMEM/F12 medium. The identity and purity of Leydig cell were assessed by 3beta-hydroxysteroid dehydrogenase delta4-delta5 isomerase (3beta-HSD). Cell viability was measured by trypan blue. Testosterone level in the medium of cultured Leydig cells was measured in various culture phases and cell density by radioimmunoassay. RESULTS: The purity of Leydig cell was (45.10 +/- 1.66)% before culture, and (81.17 +/- 2. 32)% 72 h after culture. The level of testosterone secreted by Leydig cells could be detected in the medium and its level was associated with the density and time of cultured Leydig cells. The secretion capacity of testosterone by single Leydig cell decreased gradually during the culturing period. CONCLUSION: The fetal Leydig cells isolated from fetal mice testis have high purity. It can be cultured and kept the secretion ability of testosterone for a few days in vitro. This system can provide a valuable model for further study on the cellular function of the Leydig cells of fetal mice.

Animals↗
PubMed1991

Seasonal variation in pituitary-gonadal function in free-ranging impala (Aepyceros melampus).

Blood, testicular biopsies and electroejaculates were collected from adult male impala, free-ranging in the Kruger National Park (Republic of South Africa), during the breeding (rut; April-May) and nonbreeding (September-October) seasons. Blood samples were collected at 5-min intervals for 120 min from anaesthetized males (n = 7 impala/group) treated intravenously with saline, gonadotrophin-releasing hormone (GnRH: 1 microgram/kg body weight) or human chorionic gonadotrophin (hCG: 10 or 30 iu/kg). Semen was collected from six more animals during the breeding season and 12 animals during the nonbreeding season using a standardized electroejaculation protocol. Ejaculates obtained during the nonbreeding season were of inferior quality to those collected during the breeding season, and were characterized by lower sperm concentrations, poorer sperm motility and more morphologically abnormal sperm forms. Within season, there were no differences in testosterone secretion between the two hCG doses, and these responses were similar to those observed after GnRH, but during the rut, testosterone secretion stimulated by both GnRH and hCG was approximately nine times greater than during the nonbreeding season. This seasonal increase in testosterone production was associated with a doubling in testicular volume and concentrations of luteinizing hormone (LH) receptors. Although concentrations of testicular follicle-stimulating hormone (FSH) receptors were similar between seasons, receptor content increased during rut as a result of increased testicular volume. In contrast to testosterone secretion, basal LH and FSH secretions were unaffected by season and GnRH-induced gonadotrophin secretion was reduced during rut.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats.

We investigated the effects of 8 days of LH withdrawal on rat Leydig cell peroxisomal volume, total and intraperoxisomal catalase and sterol carrier protein-2 (SCP2) contents, and LH-stimulated testosterone secretion in vitro. Three groups of adult male Sprague-Dawley rats, i.e. control, TE-implanted (testosterone-17 beta-estradiol-filled Silastic implants to suppress LH), and TELH-implanted (TE-implanted and LH replacement via Alzet mini osmotic pumps), were used. After 8 days, Leydig cell organelle volumes (stereology), intraperoxisomal catalase and SCP2 contents (immunocytochemistry), LH-stimulated testosterone secretion by isolated Leydig cells in vitro (determined by RIA), and total catalase and SCP2 contents in equal numbers of Leydig cells (immunoblot analyses) were determined. Results showed that the TELH-implanted rats were identical to controls in every parameter tested. Testis volume and Leydig cell number per testis in control and TE-implanted rats were not significantly different; however, reductions (P < 0.05) were observed in the average volume of a Leydig cell (one third of controls) and the volume of Leydig cells per testis. All Leydig cell organelle volumes tested were significantly lower in TE-implanted rats than in the controls; however, the volumes of smooth endoplasmic reticulum (SER) and peroxisomes were the most reduced (lowered to one sixth of control values). LH-stimulated testosterone secretion per Leydig cell in vitro correlated well with these changes in the volumes of Leydig cell SER and peroxisomes. Intraperoxisomal catalase in Leydig cells was unchanged in TE-implanted rats, although immunoblotting demonstrated a loss of total catalase content (which reflected the reduction in the volume of peroxisomes). SCP2 in Leydig cells of TE-implanted rats was undetectable with immunoblot analysis (explained by the reductions in Leydig cell peroxisome volume and intraperoxisomal SCP2). These results demonstrate that the organelles SER and peroxisomes and the protein SCP2 in Leydig cells are more LH dependent than the other organelles (e.g. mitochondria, lysosomes) and protein catalase, respectively. Moreover, the findings of this study are consistent with the hypothesis that Leydig cell peroxisomes play a significant role in testosterone production.

Animals↗