Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.3 (HSD)
 3,464 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present report was to study the course of development of rat Leydig cells from 17 fetal day (f.d.) up to 5 postnatal day (p.n.d.), with the help of enzymhistochemical reaction of delta 5-3 beta Hydroxysteroid-dehydrogenase (3 beta-HSDH). Testes were obtained from 17 to 21 days old embryos and from 1 to 5 days old offsprings. Cryostat sections were cut and processed for enzymhistochemical reaction of 3 beta-HSDH, employing dehydroepiandrosterone as substrate. The areas of the Leydig cells, showing the enzymatic activity, were measured morphometrically. The 3 beta-HSDH positive intertubular Leydig cells appear on 17 f.d., and grow further showing a maximum peak, relative to the size of the testis, on 19 f.d. Thereafter, the percentage of the Leydig cells relative to the size of the testis decreases continuously up to 4 p.n.d.. The Leydig cells did not regress during the period of observation. Postnatally, the large complexes disperse into many small complexes.
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PMID:Enzymhistochemical and morphometrical studies on delta 5-3 beta-hydroxysteroid dehydrogenase during the fetal and neonatal development of rat Leydig cells. 657 67

The possible effects of melatonin on testosterone and androstenedione production in vitro by testes of wild-caught bats, Scotophilus heathi, during different reproductive phases were investigated. Bats were captured during reproductive quiescent (April-August), recrudescent (September-October), breeding (November-February), and winter dormancy (late December-January) phases. Testes were incubated in media-199 for 2 h at 37 degrees C with luteinizing hormone (LH) and with or without melatonin. Melatonin had no effect on LH-induced testosterone (T) or androstenedione (A) production during the quiescent, recrudescent, and breeding phases. However, it significantly (P < 0.05) suppressed LH-induced T production but had no effect on A during winter dormancy. Testicular 17 beta-hydroxy steroid dehydrogenase (17 beta-HSD) activity was then measured in the testes from bats trapped during quiescence, breeding, and winter dormancy. Interestingly, melatonin along with LH caused suppression of 17 beta-HSD activities (3.56 +/- 0.03 unit/min/mg protein) when compared with levels of LH treated testes (7.10 +/- 1.15 unit/min/mg protein) during winter dormancy, while it had no significant effect on 17 beta-HSD activity during quiescence and breeding phases. These results suggest that in S. heathi, melatonin during winter dormancy suppresses LH-induced T production by the testes via the suppression of 17 beta-HSD activity. This may be the reason for the decline in testicular activity during winter dormancy.
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PMID:Inhibitory effects of melatonin on testosterone but not on androstenedione production during winter in the vespertilionid bat, Scotophilus heathi. 875 Mar 46

Leydig cells in the adult rat testis differentiate during the neonatal-prepubertal period. However, the stimulus for the initiation of their differentiation is still not clear. In the present study our objectives were to test the effects of thyroid hormone and LH on the initiation of precursor cell differentiation into Leydig cells in the prepubertal rat testis. Four groups of Sprague-Dawley rats were used. All treatments began at postnatal Day 1. Rats in groups I, II, and III received daily s.c. injections of saline (200 microl, controls), triiodothyronine (T(3), 50 microg/kg body weight, hyperthyroid), and LH (ovine LH 10 microg/rat/day), respectively. Rats in group IV were made hypothyroid from postnatal Day 1 by adding 0.1% propylthiouracil (PTU) to their mother's drinking water. Testes of rats were collected at 7, 8, 9, 10, 11, 12, 16, and 21 days of age, fixed in Bouin's solution, and embedded in paraffin for immunocytochemical studies. Immunoexpression of 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and LH receptors (LHR) in testicular interstitial cells (other than the fetal Leydig cells) was observed using the avidin-biotin method. In control rats, out of all spindle-shaped cell types in the testis interstitium, only the peritubular mesenchymal cells showed positive immunolabeling for 3beta-HSD, beginning from the postnatal Day 11. However, positive immunolabeling for LHR was first detected in these cells at Day 12, i.e., after acquiring the steroidogenic enzyme activity. In T(3)-treated rats 3beta-HSD positive spindle-shaped cells were first observed at Day 9 (i.e., 2 days earlier than controls), and LHR-positive cells were first observed on Day 11 (2 days later than obtaining 3beta-HSD immunoactivity); they were exclusively the peritubular mesenchymal cells. The 3beta-HSD- and LHR-positive spindle-shaped cells were absent in the testis interstitium of LH-injected rats from Days 7 through 12 but were present at postnatal Day 16. In addition, more fetal Leydig cell clusters and fetal Leydig cells in mitosis were present in LH-treated rats compared to rats in all other treatment groups. Following their first detection, the number of positive cells for each protein continued to increase at each subsequent age in controls, T(3)-, and LH-injected groups. In PTU rats, 3beta-HSD and LHR-positive spindle-shaped cells were absent throughout the experimental period. From these observations, it is possible to suggest the following regarding the developing rat testis interstitium. 1) The precursor cells for the adult generation of Leydig cells in the postnatal rat testis are the peritubular mesenchymal cells. 2) Luteinizing hormone does not initiate the onset of mesenchymal cell differentiation into Leydig cells, instead it delays this process. However, daily LH treatment causes mitosis in fetal Leydig cells and increase in fetal Leydig cell clusters. 3) Thyroid hormone is critical to initiate the onset of mesenchymal cell differentiation into adult Leydig cells.
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PMID:Effects of thyroid and luteinizing hormones on the onset of precursor cell differentiation into leydig progenitor cells in the prepubertal rat testis. 1095 37

3,3',4,4',5-Pentachlorobiphenyl (PCB126), a congener with a planar configuration, has been established to have relatively strong toxicities similar to those of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) via aryl hydrocarbon receptors. We investigated the effects of this coplanar PCB on mammalian early spermatogenesis and steroidogenesis in a mouse neonatal testicular organ culture system. Testes collected from newborn mice were subjected to organ culture in medium containing 0, 10, 100 or 1000 nM PCB126. Histochemical analysis revealed that the BrdU-labeling indices of both spermatogenic cells and Sertoli cells were unchanged in all testis specimens exposed to the coplanar PCB. CYP1A1 and steroidogenic enzymes (P450scc, P450c17, 3beta-HSD and 17beta-HSD) mRNA levels were determined by semiquantitative RT-PCR. The CYP1A1 mRNA level in cultured testis was significantly increased by PCB126 in a dose-dependent manner. Although mRNA levels of 3beta-HSD and 17beta-HSD were unchanged, the P450scc mRNA level was significantly down-regulated by PCB126 in a dose-dependent manner. In contrast, the P450c17 mRNA level was significantly higher in 1000 nM PCB126-exposed testis than in control testis. These results suggest that the coplanar PCB does not alter the proliferative activity of spermatogenic cells and Sertoli cells in neonatal testis, but that it directly affects the expression of steroidogenic enzyme genes.
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PMID:Effects of 3,3',4,4',5-pentachlorobiphenyl, a coplanar polychlorinated biphenyl congener, on cultured neonatal mouse testis. 1278 Dec 4

In ethane dimethane sulfonate (EDS)-treated adult Sprague Dawley rats, Leydig cells (LC) were not present up to 14 days but seen at 21 days. They increased in number thereafter and reached the values of age-matching controls (i.e., 150-day-old untreated) at day 60. Mesenchymal cell number per testis also increased and reached a peak at day 21, and remained at a higher (p<.05) value than the controls at days 28-60. LC were smaller at day 21, but were larger at days 28-60 (compared to untreated 90- and 150-day-old rats) and secreted more testosterone at day 60 compared to both control groups. Testes of treated rats had greater numbers of macrophages (except at day 28) and they were smaller than those in untreated rats and 60-day EDS rats. Immunolabeling studies on 3beta-HSD, 11beta-HSD1, and LH receptor activity and androgen data agreed with morphological findings. The relationship between mesenchymal and LC numbers during LC differentiation following EDS treatment is reminiscent of this process in prepubertal testis. The presence of increased numbers of macrophages in treated testes agreed with the role of macrophages on LC differentiation. The absence of aging signs in LC of 60-day treated rats who were 150 days of age can be attributed at least in part to their newly differentiated status in older rats (i.e., equivalent to pubertal LC and not to aged LC). Larger LC observed in EDS rats at days 28-60 and their increased testosterone secretory capacity at day 60 (compared to controls) are attributed to elevated plasma LH levels and locally produced factors in EDS rats.
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PMID:Effects of ethane dimethane sulfonate on the functional structure of the adult rat testis. 1285 Oct 34

Polychlorinated biphenyls (PCBs) are global pollutants of major concern to human and animal reproductive health. The present study has examined the impact of Aroclor 1254 exposure on oxidative stress and testicular Leydig cell function. Adult albino male rats of the Wistar strain were dosed for 30 days with daily intraperitoneal injections of 2 mg/kg Aroclor 1254 or vehicle (corn oil). One day after the last treatment, animals were euthanized and blood collected for the assay of serum testosterone and estradiol. Testes were removed and Leydig cells were isolated for the assay of luteinizing hormone (LH) receptors, steroidogenic enzymes cytochrome P450 side chain cleavage enzyme (P450 scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD). Cellular antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR), and glutathione-S-transferase (GST) were also assayed. Lipid peroxidation (LPO) and reactive oxygen species (ROS) were quantified. Results showed that Aroclor 1254 exposure lowered serum testosterone and estradiol levels. Leydig cell LH receptor density, activities of the steroidogenic enzymes P450 scc, 3beta-HSD, 17beta-HSD, antioxidant enzymes SOD, CAT, GPX, GR, and GST were significantly diminished whereas, LPO and ROS significantly elevated. Taken together, these results suggest that inefficient LH receptors, steroidogenic enzymes and antioxidant enzymes are possible mechanisms by which Aroclor 1254 treatment disrupts Leydig cell steroidogenesis.
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PMID:The inhibitory effects of polychlorinated biphenyl Aroclor 1254 on Leydig cell LH receptors, steroidogenic enzymes and antioxidant enzymes in adult rats. 1580 95

Free radical production and lipid peroxidation are potentially important mediators in testicular physiology and toxicology. Polychlorinated biphenyls (PCBs) are global environmental contaminants that cause disruption of the endocrine system in human and animals. The present study was conducted to elucidate the protective role of vitamin C and E against Aroclor 1254-induced changes in Leydig cell steroidogenesis and antioxidant system. Adult male rats were dosed for 30 days with daily intraperitoneal (ip) injection of 2 mg/kg Aroclor or vehicle (corn oil). One group of rats was treated with vitamin C (100 mg/kg bw/day) while the other group was treated with vitamin E (50 mg/kg bw/day) orally, simultaneously with Aroclor 1254 for 30 days. One day after the last treatment, animals were euthanized and blood was collected for the assay of serum hormones such as luteinizing hormone (LH), thyroid stimulating hormone (TSH), prolactin (PRL), triiodothyronine (T(3)), thyroxine (T(4)), testosterone and estradiol. Testes were quickly removed and Leydig cells were isolated in aseptic condition. Purity of Leydig cells was determined by 3beta-hydroxysteroid dehydrogenase (3beta-HSD) staining method. Purified Leydig cells were used for quantification of cell surface LH receptors and steroidogenic enzymes such as cytochrome P(450) side chain cleavage enzyme (P(450)scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta- HSD). Leydig cellular enzymatic antioxidants superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), gamma-glutamyl transpeptidase (gamma-GT), glutathione-S-transferase (GST) and non-enzymatic antioxidants such as vitamin C and E were assayed. Lipid peroxidation (LPO) and reactive oxygen species (ROS) were also estimated in Leydig cells. Aroclor 1254 treatment significantly reduced the serum LH, TSH, PRL, T(3), T(4), testosterone and estradiol. In addition to this, Leydig cell surface LH receptors, activities of the steroidogenic enzymes such as cytochrome P(450)scc, 3beta-HSD, 17beta-HSD, antioxidant enzymes SOD, CAT, GPX, GR, gamma-GT, GST and non-enzymatic antioxidants such as vitamin C and E were significantly diminished whereas, LPO and ROS were markedly elevated. However, the simultaneous administration of vitamin C and E in Aroclor 1254 exposed rats resulted a significant restoration of all the above-mentioned parameters to the control level. These observations suggest that vitamin C and E have ameliorative role against adverse effects of PCB on Leydig cell steroidogenesis.
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PMID:Studies on the protective role of vitamin C and E against polychlorinated biphenyl (Aroclor 1254)--induced oxidative damage in Leydig cells. 1629 53

Infertility is well-established harmful effect in chronic alcoholism and so far, there is no effective treatment for this condition. The study was conducted to determine the effects of lecithin, a known hepatoprotective on ethanol induced testicular injuries in male albino rats of Wistar strain. Five groups (n=6) of animals were used. Group I served as control. Group II received daily 1.6 g ethanol/kg body weight/day for 4 weeks orally. Group III received 1.6 g ethanol + 500 mg lecithin/kg body weight/day for four weeks orally. Group IV received 1.6 g ethanol/kg body weight for/day 4 weeks and followed by 500 mg lecithin/kg body weight/ day for four weeks orally. Group V received 1.6 g ethanol/kg body weight/ day orally for 4 weeks, followed by 4 weeks abstinence. Twenty-four hours after the last treatment the rats were sacrificed using anesthetic ether. Testes were removed and used for the estimation of extent of lipid peroxidation and tissue levels of antioxidants and steroidogenic enzymes. Lecithin protected testes from ethanol induced oxidative stress. However, the drug did not show any considerable effect on the activities of testicular delta5, 3beta-HSD and 17beta-HSD. In conclusion, ethanol induced oxidative stress can be reversed by treatment with lecithin. However the effect of lecithin on steroidogenesis was not promising.
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PMID:Effect of exogenous lecithin on ethanol-induced testicular injuries in Wistar rats. 1644 Aug 47

Exposure of neonatal testis, populated by fetal-type Leydig cells, to endocrine-active compounds may have far-reaching consequences. Our aim was to resolve the sensitivity of testosterone synthesis of infant rat (Sprague-Dawley) testis to diethylstilbestrol (DES; 0.1-1.0 mg/kg), 4-tert-octylphenol (OP; 10-100 mg/kg), and Flutamide (FLU; 2.0-25 mg/kg) given by daily sc injections from birth to postnatal day 4. Testes and serum were collected on day 14 when body and testis weight, testicular histology, circulating testosterone, LH and FSH levels, and steroidogenic acute regulatory protein (StAR) and 3beta-hydroxy-steroid-dehydrogenase (3beta-HSD) protein levels were determined. DES at each dose and FLU at 25 mg/kg dose reduced testis weight and the diameter of seminiferous cords. FLU caused some Leydig cell hyperplasia. Plasma testosterone was reduced in all DES animals, LH elevated in DES 0.5 mg/kg and FLU 25 mg/kg animals, and FSH reduced in the DES 1.0 mg/kg group. Basal testicular ex vivo progesterone and human chorionic gonadotropin (hCG)-stimulated testosterone production were decreased in DES animals. Despite a decrease in hCG-induced cyclic adenosine-3',5'-monophosphate (cAMP) production, intratesticular testosterone was increased in the FLU 10 and 25 mg/kg groups. OP 100 mg/kg elevated hCG-induced progesterone production only. No changes were seen in 3beta-HSD protein levels in any treatment group. StAR levels were reduced in DES animals. The results indicate the sensitivity of postnatal fetal-type Leydig cells to endocrine-active compounds. Suppression of StAR expression level was an early sign of the DES-induced steroidogenic lesion. FLU-induced changes suggest the importance of androgen receptor-mediated regulation of testosterone synthesis in the postnatal rat testis. Octylphenol appeared less effective in bringing about acute steroidogenic changes.
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PMID:Effects of neonatal exposure to 4-tert-octylphenol, diethylstilbestrol, and flutamide on steroidogenesis in infantile rat testis. 1653 57

Connexin43 (Cx43) is the most abundantly expressed member of the connexin (gap junction protein) family and the only one so far identified in mouse Leydig cell gap junctions. Mice lacking Cx43 were used to investigate its role in testicular androgen production and regulation. Testes from term fetuses were grafted under the kidney capsules of castrated adult males. After 3 weeks, serum from host mice was analyzed for androgens. In order to test their response to stimulation, the grafted testes were incubated in vitro with varying concentrations of LH and their androgen end products analyzed. Incubation with radiolabeled progesterone was followed by high performance liquid chromatography to quantify the androgen-intermediate metabolites. Radiolabeled testosterone in the presence of NADPH was used to determine the activity of testosterone-metabolizing enzymes 17beta-hydroxysteroid dehydrogenase (17betaHSD), 5alpha-reductase (5alphaR), and 3alpha-hydroxysteroid dehydrogenase (3alpha HSD). Serum androgen levels did not differ between hosts carrying wild-type versus null mutant grafts although Cx43-deficient testes had more 17betaHSD and 5alphaR activity than wild-type controls. Furthermore, the genotype of grafted testes did not influence LH-stimulated androgen production in vitro. These results indicate that the steroidogenic function of Leydig cells is not compromised by the absence of Cx43, perhaps because other gap junction proteins are present. Dye transfer experiments demonstrated that Cx43-deficient Leydig cells retain intercellular coupling, indicating that Cx43 is not the only protein contributing to their gap junctions. Thus, despite their prominence in Leydig cells, Cx43 gap junctions are not essential for androgen production.
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PMID:Leydig cell function in mice lacking connexin43. 1700 72


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