Effects of Prolonged Administration of Lovastatin, an Inhibitor of Cholesterol Synthesis, on the Morphology and Function of Rat Leydig Cells

Prenatal caffeine exposure adversely affects the development of the reproductive organs of male rat offspring. Thus, it is conceivable that peripubertal caffeine exposure would also influence physiologic gonadal changes and function during this critical period for sexual maturation. This study investigated the impact of high doses of caffeine on the testes of prepubertal male rats. A total of 45 immature male rats were divided randomly into three groups: a control group and 2 groups fed 120 and 180 mg/kg/day of caffeine, respectively, via the stomach for 4 weeks. Caffeine caused a significant decrease in body weight gain, accompanied by proportional decreases in lean body mass and body fat. The caffeine-fed animals had smaller and lighter testes than those of the control that were accompanied by negative influences on the histologic parameters of the testes. In addition, stimulated-testosterone ex vivo production was reduced in Leydig cells retrieved from the caffeine-fed animals. Our results demonstrate that peripubertal caffeine consumption can interfere with the maturation and function of the testis, possibly by interrupting endogenous testosterone secretion and reducing the sensitivity of Leydig cells to gonadotrophic stimulation. In addition, we confirmed that pubertal administration of caffeine reduced testis growth and altered testis histomorphology.

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Modulation of rat testes lipid composition by hormones: effect of PRL and hCG

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.255.4.e442 ◽

1988 ◽

Vol 255 (4) ◽

pp. E442-E448 ◽

Cited By ~ 1

Author(s):

E. Sebokova ◽

A. Wierzbicki ◽

M. T. Clandinin

Keyword(s):

Chorionic Gonadotropin ◽

Leydig Cells ◽

Binding Capacity ◽

Total Phospholipid ◽

Testicular Tissue ◽

Phospholipid Content ◽

Refractory State ◽

Phospholipid Ratio ◽

High Doses ◽

And Function

The effect of prolactin (PRL) and human chorionic gonadotropin (hCG) administration for 7 days on the composition and function of rat testicular plasma membrane was investigated. Refractory state in Leydig cells desensitized by hCG decreased the binding capacity for 125I-labeled hCG and also luteinizing hormone (LH)-induced adenosine 3',5'-cyclic monophosphate (cAMP) and testosterone production. In testicular membranes of hCG-treated animals, a depletion of cholesterol and an increase in total phospholipid content was observed after gonadotropin injection, thereby decreasing the cholesterol-to-phospholipid ratio. Injection of high doses of PRL had no effect on the binding capacity or affinity of the LH-hCG receptor but decreased the response of Leydig cells to LH in terms of cAMP and testosterone synthesis. PRL also increased total and esterified cholesterol and decreased free cholesterol and membrane phospholipid content. The fatty acid composition of testicular lipids was significantly and selectively influenced by both hormonal treatments. These observations suggest that metabolism of cholesterol and long-chain polyunsaturated fatty acids in testicular tissue is affected by chorionic gonadotropin and PRL and may provide the mechanism for regulating steroidogenic functions.

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Exposure to cadmium during gestation and lactation affects development and function of Leydig cells in male offspring

Environmental Toxicology ◽

10.1002/tox.22522 ◽

2017 ◽

Vol 33 (3) ◽

pp. 351-360 ◽

Cited By ~ 12

Author(s):

Huajian Tian ◽

Shaomin Chen ◽

Yang Leng ◽

Teng Li ◽

Zengli Li ◽

...

Keyword(s):

Leydig Cells ◽

Male Offspring ◽

And Function

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Effects of prolactin on the morphology and function of rat Leydig cells: short-term versus long-term administration

Cell and Tissue Research ◽

10.1007/bf00327743 ◽

1990 ◽

Vol 262 (1) ◽

pp. 41-46 ◽

Cited By ~ 2

Author(s):

Giuseppina Mazzocchi ◽

Letizia Cavallini ◽

Aldona Kasprzak ◽

Piera Rebuffat ◽

Gastone G. Nussdorfer

Keyword(s):

Leydig Cells ◽

Short Term ◽

Term Administration ◽

And Function

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Identification and Function of Putative Stem Leydig Cells in the Adult Rat Testis.

Biology of Reproduction ◽

10.1093/biolreprod/83.s1.22 ◽

2010 ◽

Vol 83 (Suppl_1) ◽

pp. 22-22

Author(s):

Haolin Chen ◽

Barry R. Zirkin

Keyword(s):

Leydig Cells ◽

Rat Testis ◽

Adult Rat ◽

And Function

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Kisspeptin/GnRH1 system in Leydig cells of horse (Equus caballus): Presence and function

Theriogenology ◽

10.1016/j.theriogenology.2020.04.006 ◽

2020 ◽

Vol 152 ◽

pp. 1-7 ◽

Cited By ~ 1

Author(s):

Linda Petrucci ◽

Margherita Maranesi ◽

Andrea Verini Supplizi ◽

Cecilia Dall’Aglio ◽

Maria Teresa Mandara ◽

...

Keyword(s):

Leydig Cells ◽

Equus Caballus ◽

And Function

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Development and Function of the Adult Generation of Leydig Cells in Mice with Sertoli Cell-Selective or Total Ablation of the Androgen Receptor

Endocrinology ◽

10.1210/en.2005-0300 ◽

2005 ◽

Vol 146 (9) ◽

pp. 4117-4126 ◽

Cited By ~ 84

Author(s):

Karel De Gendt ◽

Nina Atanassova ◽

Karen A. L. Tan ◽

Luiz Renato de França ◽

Gleydes Gambogi Parreira ◽

...

Keyword(s):

Androgen Receptor ◽

Growth Factor ◽

Sertoli Cell ◽

Leydig Cells ◽

Platelet Derived Growth Factor ◽

Testosterone Levels ◽

Androgen Action ◽

Serum Lh ◽

D 12 ◽

And Function

Abstract It is established that androgens and unidentified Sertoli cell (SC)-derived factors can influence the development of adult Leydig cells (LC) in rodents, but the mechanisms are unclear. We evaluated adult LC development and function in SC-selective androgen receptor (AR) knockout (SCARKO) and complete AR knockout (ARKO) mice. In controls, LC number increased 26-fold and LC size increased by approximately 2-fold between 12 and 140 d of age. LC number in SCARKOs was normal on d 12, but was reduced by more than 40% at later ages, although LC were larger and contained more lipid droplets and mitochondria than control LC by adulthood. ARKO LC number was reduced by up to 83% at all ages compared with controls, and LC size did not increase beyond d 12. Serum LH and testosterone levels and seminal vesicle weights were comparable in adult SCARKOs and controls, whereas LH levels were elevated 8-fold in ARKOs, although testosterone levels appeared normal. Immunohistochemistry and quantitative PCR for LC-specific markers indicated steroidogenic function per LC was probably increased in SCARKOs and reduced in ARKOs. In SCARKOs, insulin-like factor-3 and estrogen sulfotransferase (EST) mRNA expression were unchanged and increased 3-fold, respectively, compared with controls, whereas the expression of both was reduced more than 90% in ARKOs. Changes in EST expression, coupled with reduced platelet-derived growth factor-A expression, are potential causes of altered LC number and function in SCARKOs. These results show that loss of androgen action on SC has major consequences for LC development, and this could be mediated indirectly via platelet-derived growth factor-A and/or estrogens/EST.

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Cell Type-specific Expression of the Mas Proto-oncogene in Testis

Journal of Histochemistry & Cytochemistry ◽

10.1177/002215540205000510 ◽

2002 ◽

Vol 50 (5) ◽

pp. 691-695 ◽

Cited By ~ 30

Author(s):

Natalia Alenina ◽

Tatjana Baranova ◽

Eugene Smirnow ◽

Michael Bader ◽

Andrea Lippoldt ◽

...

Keyword(s):

Leydig Cells ◽

Rnase Protection Assay ◽

Cell Type ◽

Cell Type Specificity ◽

Specific Expression ◽

Rnase Protection ◽

Cell Type Specific Expression ◽

Cell Type Specific ◽

And Function ◽

Old Mice

The Mas proto-oncogene encodes a G-protein-coupled receptor with the common seven transmembrane domains and may be involved in the actions of angiotensins. Because Mas is highly expressed in testis, we investigated the cell type-specificity and the onset of expression of the gene in this organ. Using an RNase protection assay, it could be shown that neither whole testes nor cultured Sertoli and Leydig cells of 12-day-old mice express Mas mRNA. Mas expression is first detected in 18-day-old mice and thereafter increases continuously until 6 months of age. By in situ hybridization, the expression could be localized to Leydig cells and Sertoli cells, the signals being much more pronounced in the former. A weak signal was detected in primary spermatocytes. The strong ontogenetically controlled and cell type-specific expression of this membrane-bound receptor in testis implicates a role for the Mas proto-oncogene in testis maturation and function.

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Testicular steroidogenesis in the testicular feminized (Tfm) mouse: loss of 17α-hydroxylase activity

Journal of Endocrinology ◽

10.1677/joe.0.1310443 ◽

1991 ◽

Vol 131 (3) ◽

pp. 443-449 ◽

Cited By ~ 47

Author(s):

L. Murphy ◽

P. J. O'Shaughnessy

Keyword(s):

Leydig Cells ◽

Smooth Endoplasmic Reticulum ◽

Reductase Activity ◽

Serum Testosterone ◽

Normal Activity ◽

Testicular Descent ◽

Hydroxylase Activity ◽

Steroid Production ◽

And Function

ABSTRACT Testicular feminized (Tfm) mice are totally insensitive to androgen and may be used to study the role of the androgen receptor in normal development and function. We have examined testicular and Leydig cell steroidogenesis in Tfm mice. Serum bioactive LH was high in Tfm mice but serum testosterone was low and this was associated with a severe reduction in testicular testosterone production in vitro. Examination of [3H]pregnenolone metabolism by testes of Tfm mice indicated that progesterone, rather than testosterone, was the major steroid produced. Leydig cells were isolated from normal and Tfm mice and from normal mice in which testicular descent was surgically prevented before puberty. As in whole testes, androgen production in response to human chorionic gonadotrophin was severely reduced in Leydig cells from testes of Tfm mice compared with normal or cryptorchid groups. In contrast, progesterone production by Leydig cells from testes of Tfm mice was markedly increased in comparison with other groups. Total steroid production (progesterone plus androstenedione plus testosterone), however, was only 24% of normal in Leydig cells from Tfm mice. The pattern of steroid production by Leydig cells from cryptorchid testes was similar to control, although total steroid production was reduced to about 50% (this was significantly higher than the Tfm group, P<0·05). The high progesterone/androgen ratio in testes from Tfm mice suggested that 17α-hydroxylase was depleted in these animals. To confirm this, activity of the four major steroidogenic enzymes associated with the smooth endoplasmic reticulum was measured. Activities (per testis) of 3β-hydroxysteroid dehydrogenase and 5α-reductase were normal in Tfm and cryptorchid mice but, as expected, 17α-hydroxylase activity was only 2·4% of control and 4·5% of cryptorchid testes. 17-Ketosteroid reductase activity was markedly reduced in cryptorchid testes (14·4% of control) but there was a further reduction in testes from Tfm mice to 0·1% of control. Results show that the Tfm mutation is associated with marked loss of 17α-hydroxylase and 17-ketosteroid reductase activities. This suggests that these enzymes may require receptor-mediated androgen stimulation during development to express normal activity. Journal of Endocrinology (1991) 131, 443–449

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Glucocorticoids Affect Male Testicular Steroidogenesis

Physiological Research ◽

10.33549/physiolres.934508 ◽

2020 ◽

pp. S205-S210

Author(s):

R. HAMPL ◽

L. STÁRKA

Keyword(s):

Leydig Cells ◽

Glucocorticoid Receptors ◽

Molecular Mechanisms ◽

Target Cells ◽

Clinical Effects ◽

Steroid Production ◽

Glucocorticoid Treatment ◽

Testicular Steroidogenesis ◽

And Function

Through their receptors at each level of hypothalamo-pituitary-gonadal axis glucocorticoid excess, either endogenous or administered or stress-induced, could affect steroid production in the testis and thus male fertility. The main ways by which glucocorticoids act are as follows: 1) Affecting gonadoliberin and LH synthesis and release through glucocorticoid receptors in hypothalamic neurons and pituitary gonadotropes. 2) By so far not clearly evidenced reduction of the number of LH receptors on the membrane of Leydig cells. 3) By affecting expression and function of steroidogenic enzymes in the testis. 4) By regulation of in situ access of glucocorticoid to its target cells in the testis. 5) By promotion Leydig cell apoptosis. The review provides a survey of physiological and molecular mechanisms staying behind these effects. It does not deal with the clinical effects of glucocorticoid treatment which would substantially exceed the scope of the pater.

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