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Journal articles on the topic 'Testicular steroidogenesis'

Author: Grafiati
Published: 19 February 2023

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1

Rommerts, F. F. G., K. Teerds, A. P. N. Themmen, and M. van Noort. "Multiple regulation of testicular steroidogenesis." Journal of Steroid Biochemistry 27, no. 1-3 (January 1987): 309–16. http://dx.doi.org/10.1016/0022-4731(87)90322-0.

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2

Sarawi, Wedad S., Ahlam M. Alhusaini, Laila M. Fadda, Hatun A. Alomar, Awatif B. Albaker, Hanan K. Alghibiwi, Amjad S. Aljrboa, Areej M. Alotaibi, Iman H. Hasan, and Ayman M. Mahmoud. "Nano-Curcumin Prevents Copper Reproductive Toxicity by Attenuating Oxidative Stress and Inflammation and Improving Nrf2/HO-1 Signaling and Pituitary-Gonadal Axis in Male Rats." Toxics 10, no. 7 (June 30, 2022): 356. http://dx.doi.org/10.3390/toxics10070356.

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Copper is essential for several cellular processes and is an important catalytic factor for many proteins. However, excess copper can provoke oxidative stress and reproductive toxicity. This study evaluated the effect of liposomal nano-curcumin (N-CUR) and CUR on testicular oxidative injury, inflammation, and apoptosis, and altered steroidogenesis and Nrf2/HO-1 signaling induced by copper sulfate (CuSO4). Rats received CuSO4 and N-CUR or CUR via oral gavage for 7 days. CuSO4 induced histopathological changes and altered pituitary-gonadal axis manifested by decreased serum gonadotropins and testosterone. Testicular steroidogenesis genes (StAR, 3β-HSD, CYP17A1, and 17β-HSD) and androgen receptor (AR) were downregulated in rats that received CuSO4. N-CUR and CUR prevented testicular tissue injury, increased circulating FSH, LH, and testosterone, and upregulated testicular steroidogenesis genes and AR. Additionally, N-CUR and CUR decreased testicular MDA, NO, NF-κB, iNOS, TNF-α, Bax, and caspase-3 while enhanced Bcl-2, Nrf2, and the antioxidants GSH, HO-1, SOD, and catalase. In conclusion, N-CUR and CUR prevented CuSO4-induced reproductive toxicity in male rats by suppressing oxidative injury and inflammatory response and boosting steroidogenesis, sex hormones, and Nrf2/HO-1 signaling. N-CUR was more effective in ameliorating tissue injury, oxidative stress, inflammation, and apoptosis and enhancing steroidogenesis and Nrf2/HO-1 than the native form.
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3

Bakhtyukov, Andrey A., Kira V. Derkach, Maxim A. Gureev, Dmitry V. Dar’in, Viktor N. Sorokoumov, Irina V. Romanova, Irina Yu Morina, Anna M. Stepochkina, and Alexander O. Shpakov. "Comparative Study of the Steroidogenic Effects of Human Chorionic Gonadotropin and Thieno[2,3-D]pyrimidine-Based Allosteric Agonist of Luteinizing Hormone Receptor in Young Adult, Aging and Diabetic Male Rats." International Journal of Molecular Sciences 21, no. 20 (October 11, 2020): 7493. http://dx.doi.org/10.3390/ijms21207493.

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Low-molecular-weight agonists of luteinizing hormone (LH)/human chorionic gonadotropin (hCG) receptor (LHCGR), which interact with LHCGR transmembrane allosteric site and, in comparison with gonadotropins, more selectively activate intracellular effectors, are currently being developed. Meanwhile, their effects on testicular steroidogenesis have not been studied. The purpose of this work is to perform a comparative study of the effects of 5-amino-N-tert-butyl-4-(3-(1-methylpyrazole-4-carboxamido)phenyl)-2-(methylthio)thieno[2,3-d] pyrimidine-6-carboxamide (TP4/2), a LHCGR allosteric agonist developed by us, and hCG on adenylyl cyclase activity in rat testicular membranes, testosterone levels, testicular steroidogenesis and spermatogenesis in young (four-month-old), aging (18-month-old) and diabetic male Wistar rats. Type 1 diabetes was caused by a single streptozotocin (50 mg/kg) injection. TP4/2 (20 mg/kg/day) and hCG (20 IU/rat/day) were administered for 5 days. TP4/2 was less effective in adenylyl cyclase stimulation and ability to activate steroidogenesis when administered once into rats. On the 3rd–5th day, TP4/2 and hCG steroidogenic effects in young adult, aging and diabetic rats were comparable. Unlike hCG, TP4/2 did not inhibit LHCGR gene expression and did not hyperstimulate the testicular steroidogenesis system, moderately increasing steroidogenic proteins gene expression and testosterone production. In aging and diabetic testes, TP4/2 improved spermatogenesis. Thus, during five-day administration, TP4/2 steadily stimulates testicular steroidogenesis, and can be used to prevent androgen deficiency in aging and diabetes.
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4

Marak, Chuckles Ch, Brilliant N. Marak, Ved Prakash Singh, Guruswami Gurusubramanian, and Vikas Kumar Roy. "Effect of Cycas pectinata Seed Extract on Testicular Steroidogenesis in a Mouse Model." Andrologia 2023 (February 9, 2023): 1–15. http://dx.doi.org/10.1155/2023/5446928.

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The seed of Cycas pectinata is widely used in traditional practices in the Northeastern region of India for diverse purposes along with improving testicular functions. Thus, it may be hypothesized that the phytochemicals of C. pectinata seed could modulate testicular steroidogenesis. Therefore, we have investigated the effects of C. Pectinata seed extract (CPE) on testicular steroidogenesis by using in vivo and in vitro approaches. We have also performed the molecular docking of phytochemicals with some steroidogenic markers based on the identified phytochemicals from our previous study. The in vivo treatment of CPE increased the circulating estrogen and decreased circulating testosterone. The in vitro treatment of CPE also showed increased secretion of estrogen which can be suggested due to an increase in the aromatase (CYP19A1) activity. Our results also showed that the expression and localization of CYP19A1 were elevated by the CPE. The treatment of CPE also showed an accumulation of cholesterol in the testis, which could enhance testicular steroidogenesis. The other steroidogenic markers like 3βHSD, StAR, and LHR were upregulated by the CPE. Twelve compounds exhibited binding energy in the range of -10.0 to -8.0 kcal/mol with CYP19A1. Our data from in vitro, in vivo, and docking studies, showed that phytochemicals of CPE could modulate testicular steroidogenesis.
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5

Alam, Mohammad Shah, Seiichiroh Ohsako, Takashi Matsuwaki, Xiao Bo Zhu, Naoki Tsunekawa, Yoshiakira Kanai, Hideko Sone, Chiharu Tohyama, and Masamichi Kurohmaru. "Induction of spermatogenic cell apoptosis in prepubertal rat testes irrespective of testicular steroidogenesis: a possible estrogenic effect of di(n-butyl) phthalate." REPRODUCTION 139, no. 2 (February 2010): 427–37. http://dx.doi.org/10.1530/rep-09-0226.

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Although di(n-butyl) phthalate (DBP), a suspected endocrine disruptor, induces testicular atrophy in prepubertal male rats, whether it exerts estrogenic activity in vivo remains a matter of debate. In the present study, we explored the estrogenic potency of DBP using 3-week-old male rats, and then examined the relationship between estrogen-induced spermatogenic cell apoptosis and testicular steroidogenesis. Daily exposure to DBP for 7 days caused testicular atrophy due to loss of spermatogenic cells, whereas testicular steroidogenesis was almost the same with the control values. A single exposure of DBP decreased testicular steroidogenesis in addition to decreasing the level of serum LH at 3 h after DBP treatment, with an extremely high incidence of apoptotic spermatogenic cells at 6 h after administration. To elucidate the estrogenic activity of DBP, we carried out an inhibition study using pure antiestrogen ICI 182,780 (ICI) in a model of spermatogenic cell apoptosis induced by DBP or estradial-3-benzoate (EB). Although both the DBP- and EB-treated groups showed a significant increase in spermatogenic cell apoptosis, ICI pretreatment significantly decreased the number of apoptotic spermatogenic cells in these two groups. In contrast, testicular steroidogenesis and serum FSH were significantly reduced in all the treated groups, even in the DBP+ICI and EB+ICI groups. Taken together, these findings led us to conclude that estrogenic compounds such as DBP and EB induce spermatogenic cell apoptosis in prepubertal rats, probably by activating estrogen receptors in testis, and that reduction in testicular steroidogenic function induced by estrogenic compounds is not associated with spermatogenic cell apoptosis.
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6

Kostic, TS, SA Andric, D. Maric, SS Stojilkovic, and R. Kovacevic. "Involvement of inducible nitric oxide synthase in stress-impaired testicular steroidogenesis." Journal of Endocrinology 163, no. 3 (December 1, 1999): 409–16. http://dx.doi.org/10.1677/joe.0.1630409.

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The immobilization stress induces an acute inhibition of testicular steroidogenesis that is mediated by the nitric oxide (NO) signaling pathway. Here we compared the effects of 2-h immobilization stress on in vivo and in vitro rat steroidogenesis at two time points, 0 h and 6 h after the end of the stress session. As expected, serum androgens and human chorionic gonadotropin (hCG)-stimulated progesterone and testosterone production by testicular tissue were inhibited at 0 h, and also at the 6-h time point. Both the acute and sustained inhibitions of in vitro steroidogenesis were accompanied by a significant increase in nitrite, a stable oxidation product of NO. To clarify which subtype of NO synthase (NOS) (constitutive (cNOS) or inducible (iNOS)) participates in down-regulation of testicular steroidogenesis, aminoguanidine hydrochloride (AG), a selective iNOS inhibitor, was employed. Intratesticular injection of AG prevented the sustained, but not the acute, stress-induced decrease in serum testosterone. When added in vitro, it also prevented the sustained decrease in steroid production and increase in nitrite production by testicular tissue, both in a dose-dependent manner and with EC microM. Furthermore, AG added in vivo and in vitro effectively blocked the sustained decrease in 3beta-hydroxysteroid dehydrogenase (3betaHSD) and 17alpha-hydroxylase/C17-20 lyase (P450c17) activities. In all concentrations employed, AG did not affect serum androgens and in vitro steroid and nitrite production in unstressed animals. These results indicate that the NO signaling pathway participates in acute and sustained stress-induced down-regulation of testicular steroidogenesis, presumably through its direct action on 3betaHSD and P450c17. The acute NO production is controlled by cNOS and the sustained production of this messenger is controlled by iNOS.
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7

Rossato, M., G. Guarneri, T. Lavagnini, D. Padovan, and C. Foresta. "Simvastatin Influences Testicular Steroidogenesis in Human." Hormone and Metabolic Research 25, no. 09 (September 1993): 503–5. http://dx.doi.org/10.1055/s-2007-1002161.

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8

Kovačević, R., L. Krsmanović, S. Cupać, I. Simonović, S. Stojilković, D. Marić, and R. K. Andjus. "Effects of bromocriptine on testicular steroidogenesis." Journal of Steroid Biochemistry 25 (January 1986): 41. http://dx.doi.org/10.1016/0022-4731(86)90578-9.

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9

Ahmed, Mona M., Mohamed M. A. Hussein, Taisir Saber, and Yasmina M. Abd-Elhakim. "Palliative Effect of Resveratrol against Nanosized Iron Oxide-Induced Oxidative Stress and Steroidogenesis-Related Genes Dysregulation in Testicular Tissue of Adult Male Rats." International Journal of Environmental Research and Public Health 19, no. 13 (July 4, 2022): 8171. http://dx.doi.org/10.3390/ijerph19138171.

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The nano-sized iron oxide (Fe2O3-NPs) is one of the most used engineered nanomaterials worldwide. This study investigated the efficacy of natural polyphenol resveratrol (RSV) (20 mg/kg b.wt, orally once daily) to alleviate the impaired sperm quality and testicular injury resulting from Fe2O3-NPs exposure (3.5 or 7 mg/kg b.wt, intraperitoneally once a week) for eight weeks. Spermiograms, sexual hormonal levels, oxidative stress indicators, and lipid peroxidation biomarker were assessed. Moreover, the steroidogenesis-related genes mRNA expressions were evaluated. The results showed that RSV substantially rescued Fe2O3-NPs-mediated sperm defects. Additionally, the Fe2O3-NPs-induced depressing effects on sperm motility and viability were markedly counteracted by RSV. Moreover, RSV significantly restored Fe2O3-NPs-induced depletion of testosterone, follicle-stimulated hormone, luteinizing hormone, and testicular antioxidant enzymes but reduced malondialdehyde content. Furthermore, the Fe2O3-NPs-induced downregulation of steroidogenesis-related genes (3 β-HSD, 17 β-HSD, and Nr5A1) was significantly counteracted in the testicular tissue of RSV-treated rats. These findings concluded that RSV could limit the Fe2O3-NPs-induced reduced sperm quality and testicular injury most likely via their antioxidant activity and steroidogenesis-related gene expression modulation.
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10

Park, Eunsook, Yeawon Kim, Hyun Joo Lee, and Keesook Lee. "Differential Regulation Of Steroidogenic Enzyme Genes by TRα Signaling in Testicular Leydig Cells." Molecular Endocrinology 28, no. 6 (June 1, 2014): 822–33. http://dx.doi.org/10.1210/me.2013-1150.

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Abstract Thyroid hormone signaling has long been implicated in mammalian testicular function, affecting steroidogenesis in testicular Leydig cells. However, its molecular mechanism is not well understood. Here, we investigated the molecular action of thyroid hormone receptor-α (TRα) on mouse testicular steroidogenesis. TRα/thyroid hormone (T3) signaling differentially affected the expression of steroidogenic enzyme genes, mainly regulating their promoter activity. TRα directly regulated the promoter activity of the cytochrome P450 17α-hydroxylase/C17–20 lyase gene, elevating its expression in the presence of T3. TRα also indirectly regulated the expression of steroidogenic enzyme genes, such as steroidogenic acute regulatory protein and 3β-hydroxysteroid dehydrogenase, by modulating the transactivation of Nur77 on steroidogenic enzyme gene promoters through protein-protein interaction. TRα enhanced Nur77 transactivation by excluding histone deacetylases from Nur77 in the absence of T3, whereas liganded TRα inhibited Nur77 transactivation, likely due to interfering with the recruitment of coactivator such as the steroid receptor coactivator-1 to Nur77. Together, these findings suggest a role of TRα/T3 in testicular steroidogenesis and may provide molecular mechanisms for the differential regulation of steroidogenic enzyme genes by thyroid hormone.
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11

MARAN, R. R. M. "THYROID HORMONES: THEIR ROLE IN TESTICULAR STEROIDOGENESIS." Archives of Andrology 49, no. 5 (January 2003): 375–88. http://dx.doi.org/10.1080/01485010390204968.

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12

Maran, R. R. M. "THYROID HORMONES: THEIR ROLE IN TESTICULAR STEROIDOGENESIS." Archives of Andrology 49, no. 5 (September 2003): 375–88. http://dx.doi.org/10.1080/713828213.

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13

Lim, Audrey, Vineet Kumar, Shantala A. Hari Dass, and Ajai Vyas. "Toxoplasma gondiiinfection enhances testicular steroidogenesis in rats." Molecular Ecology 22, no. 1 (November 28, 2012): 102–10. http://dx.doi.org/10.1111/mec.12042.

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14

Hales, Dale Buchanan. "Testicular macrophage modulation of Leydig cell steroidogenesis." Journal of Reproductive Immunology 57, no. 1-2 (October 2002): 3–18. http://dx.doi.org/10.1016/s0165-0378(02)00020-7.

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15

Bartke, A., A. G. Amador, V. Chandrashekar, and H. G. Klemcke. "Seasonal differences in testicular receptors and steroidogenesis." Journal of Steroid Biochemistry 27, no. 1-3 (January 1987): 581–87. http://dx.doi.org/10.1016/0022-4731(87)90357-8.

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16

SUESCUN, MARÍA O., CARLOS SCORTICATI, VIOLETA A. CHIAUZZI, HÉCTOR E. CHEMES, MARCO A. RIVAROLA, and RICARDO S. CALANDRA. "Induced Hypoprolactinemia and Testicular Steroidogenesis in Man." Journal of Andrology 6, no. 1 (January 2, 1985): 10–14. http://dx.doi.org/10.1002/j.1939-4640.1985.tb00811.x.

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17

Han, Dae-Yong, Sang-Rim Kang, Oh-Sung Park, Jae-Hyeon Cho, Chung-Kil Won, Hyeon-Soo Park, Kwang-Il Park, Eun-Hee Kim, and Gon-Sup Kim. "Polychlorinated biphenyls have inhibitory effect on testicular steroidogenesis by downregulation of P45017α and P450scc." Toxicology and Industrial Health 26, no. 5 (March 31, 2010): 287–96. http://dx.doi.org/10.1177/0748233710364961.

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Polychlorinated biphenyls (PCBs) are environmental pollutants that are quite toxic to biological systems. This study examined the inhibitory effect of PCB126 and PCB114 on testicular steroidogenesis in male rats. Male Sprague Dawley rats received weekly intraperitoneal injections of PCB126 (0.2 mg/kg) or PCB114 (20 mg/kg) or vehicle (corn oil). Animals from each group were sacrificed at 2, 5 and 8 weeks after the injections. Blood and testis tissue samples were collected for the hormone assay, Western blotting and reverse transcriptase polymerase chain reaction (RT-PCR). The testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were assayed, and the expression levels of the mRNA and proteins associated with the testosterone biosynthesis pathway were measured to determine the effect of PCB126 and PCB114 on testicular steroidogenesis. The results showed that the testis weight was significantly higher in the PCB126-treated rats given eight shots. Moreover, the serum testosterone levels were significantly lower in the PCB126 and PCB114-treated groups than the control. The transcription and translation levels of P45017α and P450scc were significantly lower in the PCB126-treated groups than the control. These results suggest that PCB126 may affect testicular steroidogenesis by downregulating P45017α, P450 scc and have inhibitory effect on the testicular functions.
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18

Bassi, Geetika, and Suresh Mishra. "Prohibitin-1 Transgenic Mice Revealed an Important Role of Prohibitin in Testicular Steroidogenesis." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A771. http://dx.doi.org/10.1210/jendso/bvab048.1568.

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Abstract Testosterone, the male sex hormone, plays an important role in the sexual development and fertility. Consequently, its deficiency causes infertility, obesity, osteoporosis and cardiovascular diseases. Leydig cells (LCs) are the testicular interstitial cells responsible for the biosynthesis of testosterone in response to luteinizing hormone (LH) from the pituitary. Cholesterol is the essential substrate for steroidogenesis which is translocated from the cytosol to the mitochondria where it gets converted to pregnenolone (by P450 side chain cleavage enzyme). Subsequently, pregnenolone translocate to endoplasmic reticulum where action of various enzymes results in the biosynthesis of testosterone. Prohibitin-1 (PHB1) is an evolutionary conserved ubiquitously expressed protein with cell compartment and cell-type specific functions. Mitochondrial function of PHB1 has been widely studied but its role in testicular steroidogenesis is unexplored. Recently, we have reported two transgenic mice models of PHB1, PHB-Tg and mutant-PHB-Tg (mPHB-Tg), expressing PHB1 or Y114F (mutant PHB1) respectively under the control of Fabp-4 gene promoter. During phenotypic characterization of these mice models, we observed a drastic size/weight difference in the testis of PHB-Tg and mPHB-Tg when compared with wild type mice. The mPHB-Tg mice testis was significantly smaller than the PHB-Tg and wild type mice. Further analysis of mPHB-Tg testis revealed wider testicular interstitium with LC hyperplasia and elongated seminiferous tubules. Ultrastructure investigation revealed that LCs of mPHB-Tg mice have prominent nucleus with increased number of mitochondria and lipid droplets. In addition, electron microscopic images of mPHB-Tg mice LCs revealed a sign of lipophagy and mitophagy. This prompted us to measure testosterone levels in these mice; surprisingly mPHB-Tg mice showed significantly higher testosterone levels as compared to PHB-Tg and wild type mice. Furthermore, testicular lysates and primary LCs cell lysates from transgenic mice models revealed that overexpression of PHB/mPHB in LCs inversely effect expression levels of steroidogenic acute regulatory protein (StAR). Moreover, co-immunoprecipitation of PHB1 displayed an interaction with StAR, P450scc and LC3 further revealing a key role of PHB1 in cholesterol translocation, testicular steroidogenesis and autophagy. Taken together, this finding suggests that PHB1 plays a multifaceted role in testicular steroidogenesis from determining testis size to the translocation of cholesterol into the mitochondria, in maintaining lipid homeostasis and biosynthesis of testosterone. Implications of our findings are broad because cholesterol translocation to the mitochondria and its subsequent utilization for steroidogenesis is conserved in all steroidogenic tissues.
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19

Foresta, Carlo, Roberto Mioni, Paola Bordon, Francesco Gottardello, Andrea Nogara, and Marco Rossato. "Erythropoietin and testicular steroidogenesis: the role of second messengers." European Journal of Endocrinology 132, no. 1 (January 1995): 103–8. http://dx.doi.org/10.1530/eje.0.1320103.

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Foresta C, Mioni R, Bordon P, Gottardello F, Nogara A, Rossato M. Erythropoietin and testicular steroidogenesis: the role of second messengers. Eur J Endocrinol 1995;132:103–8. ISSN 0804–4643 It has been demonstrated that erythropoietin (EPO) influences rat and human Leydig cell steroidogenesis, stimulating testosterone production through a direct and specific receptor-mediated mechanism. The aim of this study was to investigate the mechanism by which recombinant human erythropoietin (rHuEPO) exerts its stimulatory effect on rat Leydig cells. Recombinant human EPO did not induce, at any dose tested (10−10 to 10−13 mol/l), an increase in either cAMP or cGMP, suggesting that in Leydig cells the effect of rHuEPO does not involve the adenylate or guanylate–cyclase systems. The role of transmembrane calcium flux in rHuEPO-stimulated steroidogenesis was studied by evaluating the effect of calcium channel blocker, verapamil, and by the 45Ca2+ uptake method. Verapamil did not influence rHuEPO-induced testosterone secretion and rHuEPO did not modify calcium recycling, indicating that calcium transmembrane flux is not involved in the rHuEPO effect. The protein kinase C inhibitor staurosporine (10, 30, 100 and 300 nmol/l) inhibited rHuEPO-stimulated testicular steroidogenesis in a dose-dependent manner. This indirect evidence suggests that the stimulatory effect of rHuEPO on rat Leydig cells may involve protein kinase C activation. Carlo Foresta, Institute of Internal Medicine, Via Ospedale Civile 105, 35128 Padova, Italy
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20

Sharma, Aditi, Thilipan Thaventhiran, Suks Minhas, Waljit S. Dhillo, and Channa N. Jayasena. "Kisspeptin and Testicular Function—Is It Necessary?" International Journal of Molecular Sciences 21, no. 8 (April 22, 2020): 2958. http://dx.doi.org/10.3390/ijms21082958.

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The role of kisspeptin in stimulating hypothalamic GnRH is undisputed. However, the role of kisspeptin signaling in testicular function is less clear. The testes are essential for male reproduction through their functions of spermatogenesis and steroidogenesis. Our review focused on the current literature investigating the distribution, regulation and effects of kisspeptin and its receptor (KISS1/KISS1R) within the testes of species studied to date. There is substantial evidence of localised KISS1/KISS1R expression and peptide distribution in the testes. However, variability is observed in the testicular cell types expressing KISS1/KISS1R. Evidence is presented for modulation of steroidogenesis and sperm function by kisspeptin signaling. However, the physiological importance of such effects, and whether these are paracrine or endocrine manifestations, remain unclear.
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21

Kim, Hansle, Sudeep Kumar, and Keesook Lee. "FOXA3, a Negative Regulator of Nur77 Expression and Activity in Testicular Steroidogenesis." International Journal of Endocrinology 2021 (March 3, 2021): 1–8. http://dx.doi.org/10.1155/2021/6619447.

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Biosynthesis of testosterone occurs mainly in the testicular Leydig cells. Nur77, an orphan nuclear receptor that is expressed in response to the luteinizing hormone/cyclic adenosine monophosphate (LH/cAMP) signaling pathway, is one of the key factors that regulate steroidogenesis in Leydig cells. The function of Nur77 is modulated through interaction with other proteins. FOXA3, a transcription factor that is crucial for male fertility, is also expressed in Leydig cells. Here, we sought to elucidate the role of FOXA3 in testicular steroidogenesis by focusing on its interaction with Nur77. LH/cAMP signaling induces the onset of steroidogenesis in Leydig cells but has a repressive effect on the expression of FOXA3. Overexpression of FOXA3 in MA-10 Leydig cells repressed cAMP-induced expression of Nur77 and its target steroidogenic genes (StAR, P450c17, and Hsd3β). Furthermore, FOXA3 suppressed Nur77 transactivation of the promoter of steroidogenic genes. In mouse primary Leydig cells, adenovirus-mediated overexpression of FOXA3 had similar effects and resulted in decreased production of testosterone. Taken together, these results suggest the role of FOXA3 in the regulation of steroidogenic genes in Leydig cells and fine-tuning steroidogenesis in the testis.
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22

Elrashidy, Rania A., Esraa M. Zakaria, Asmaa M. Elmaghraby, Rasha E. M. Abd El Aziz, Ranya M. Abdelgalil, Rehab M. Megahed, Asmaa A. Elshiech, Doaa E. A. Salama, and Samah E. Ibrahim. "Linagliptin and Vitamin D3 Synergistically Rescue Testicular Steroidogenesis and Spermatogenesis in Cisplatin-Exposed Rats: The Crosstalk of Endoplasmic Reticulum Stress with NF-κB/iNOS Activation." Molecules 27, no. 21 (October 27, 2022): 7299. http://dx.doi.org/10.3390/molecules27217299.

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This study investigated the therapeutic effect of linagliptin and/or vitamin D3 on testicular steroidogenesis and spermatogenesis in cisplatin-exposed rats including their impact on endoplasmic reticulum (ER) stress and NF-κB/iNOS crosstalk. Cisplatin (7 mg/kg, IP) was injected into adult male albino rats which then were orally treated with drug vehicle, linagliptin (3 mg/kg/day), vitamin D3 (10 μg/kg/day) or both drugs for four weeks. Age-matched rats were used as the control group. Serum samples and testes were collected for further analyses. Cisplatin induced testicular weight loss, deteriorated testicular architecture, loss of germ cells and declined serum and intra-testicular testosterone levels, compared to the control group. There was down-regulation of steroidogenic markers including StAR, CYP11A1, HSD3b and HSD17b in cisplatin-exposed rats, compared with controls. Cisplatin-exposed rats showed up-regulation of ER stress markers in testicular tissue along with increased expression of NF-κB and iNOS in spermatogenic and Leydig cells. These perturbations were almost reversed by vitamin D3 or linagliptin. The combined therapy exerted a more remarkable effect on testicular dysfunction than either monotherapy. These findings suggest a novel therapeutic application for linagliptin combined with vitamin D3 to restore testicular architecture, aberrant steroidogenesis and spermatogenesis after cisplatin exposure. These effects may be attributed to suppression of ER stress and NF-kB/iNOS.
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23

Santos, P. R. S., F. D. Oliveira, M. A. M. Arroyo, M. F. Oliveira, P. Castelucci, A. J. Conley, and A. C. Assis Neto. "Steroidogenesis during postnatal testicular development of Galea spixii." Reproduction 154, no. 5 (November 2017): 645–52. http://dx.doi.org/10.1530/rep-17-0075.

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The androgen/estrogen balance is essential for normal sexual development and reproduction in mammals. Studies performed herein investigated the potential for estrogen synthesis in cells of the testes of a hystricomorph rodent, Galea spixii. The study characterized the expression of the key enzymes responsible for estrogen and androgen synthesis, cytochromes P450 aromatase (P450arom), 17α-hydroxylase/17,20-lyase (P450c17) respectively, as well as the redox partner NADPH cytochrome P450 oxido-reductase (CPR) required to support electron transfer and catalysis of these P450s, by immunohistochemistry (IHC) and quantitative polymerase chain reaction (qPCR) analysis, throughout postnatal sexual development. Testes (immature, pre-pubertal, pubertal and post-pubertal) were collected, fixed for IHC (CYP19, CYP17 and CPR) and stored frozen for qPCR for the relevant gene transcripts (Cyp19a1 and Cyp17a1). Expression of P450c17 was significantly elevated at the pre-pubertal and pubertal stages. Based on IHC, P450c17 was expressed only in Leydig cell clusters. The expression of P450arom was detectable at all stages of sexual development of Galea spixii. IHC data suggest that estrogen synthesis was not restricted to somatic cells (Leydig cells/Sertoli cells), but that germ cells may also be capable of converting androgens into estrogens, important for testicular function and spermatogenesis.
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O'SHAUGHNESSY, P. J., D. H. ABBOTT, A. J. LEIGH, and B. M. CATTANACH. "Testicular steroidogenesis in X/X sex-reversed mice." International Journal of Andrology 14, no. 2 (April 1991): 140–48. http://dx.doi.org/10.1111/j.1365-2605.1991.tb01075.x.

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Wu, F. C. W. "7 Testicular steroidogenesis and androgen use and abuse." Baillière's Clinical Endocrinology and Metabolism 6, no. 2 (April 1992): 373–403. http://dx.doi.org/10.1016/s0950-351x(05)80155-7.

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Kannan, Arun, Antojenifer Panneerselvam, Lezy Flora Mariajoseph-Antony, Chithra Loganathan, and Chidambaram Prahalathan. "Role of Aquaporins in Spermatogenesis and Testicular Steroidogenesis." Journal of Membrane Biology 253, no. 2 (March 26, 2020): 109–14. http://dx.doi.org/10.1007/s00232-020-00114-5.

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RAY, A., S. CHATTERJEE, P. BAGCHI, T. K. DAS, and C. DEB. "Effect of Quinalphos on Testicular Steroidogenesis in Rats." Andrologia 20, no. 2 (April 24, 2009): 163–68. http://dx.doi.org/10.1111/j.1439-0272.1988.tb00682.x.

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B, Lal. "INTRA-TESTICULAR NITRIC OXIDE REGULATES STEROIDOGENESIS IN FISH." Indian Journal of Science and Technology 4, si1 (June 20, 2011): 136. http://dx.doi.org/10.17485/ijst/2011/v4is.75.

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Verma, Rachna, and Amitabh Krishna. "Effect of tamoxifen on spermatogenesis and testicular steroidogenesis." Biochemical and Biophysical Research Communications 486, no. 1 (April 2017): 36–42. http://dx.doi.org/10.1016/j.bbrc.2017.02.092.

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Geng, Xu-Jing, Dong-Mei Zhao, Gen-Hong Mao, and Li Tan. "MicroRNA-150 regulates steroidogenesis of mouse testicular Leydig cells by targeting STAR." Reproduction 154, no. 3 (September 2017): 229–36. http://dx.doi.org/10.1530/rep-17-0234.

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Leydig cells are essential for male reproductive development throughout life. Production of androgens as well as intermediate steroids is tightly regulated. Although microRNAs (miRNAs) are suggested to play important roles in spermatogenesis, little is currently known regarding the regulation of steroidogenesis by miRNAs in Leydig cells. Here, we found that miR-150 was predominantly expressed in Leydig cells within mouse testis. Therefore, we determined steroidogenesis of the Leydig cells in which miR-150 was knocked down or overexpressed using miR-150 antagomir and agomir, respectively. Compared with negative control group, a significant increase of STAR expression was observed in miR-150 antagomir-treated Leydig cells. Conversely, STAR expression was significantly reduced in miR-150 agomir-transfected Leydig cells. Production of sex-steroid precursors and testosterone of Leydig cells was also negatively controlled by miR-150. We further identifiedStaras a target of miR-150 using luciferase reporter assay. Finally, we confirmed that miR-150 was necessary for steroidogenesis and spermatogenesisin vivovia intratesticular injection of miR-150 antagomir or agomir. Taken together, our studies suggest that miR-150 negatively regulates the expression of STAR and steroidogenesis of Leydig cells in mice.
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Bakhtyukov, Andrey A., Kira V. Derkach, Viktor N. Sorokoumov, Anna M. Stepochkina, Irina V. Romanova, Irina Yu Morina, Irina O. Zakharova, Liubov V. Bayunova, and Alexander O. Shpakov. "The Effects of Separate and Combined Treatment of Male Rats with Type 2 Diabetes with Metformin and Orthosteric and Allosteric Agonists of Luteinizing Hormone Receptor on Steroidogenesis and Spermatogenesis." International Journal of Molecular Sciences 23, no. 1 (December 24, 2021): 198. http://dx.doi.org/10.3390/ijms23010198.

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In men with type 2 diabetes mellitus (T2DM), steroidogenesis and spermatogenesis are impaired. Metformin and the agonists of luteinizing hormone/human chorionic gonadotropin(hCG)-receptor (LH/hCG-R) (hCG, low-molecular-weight allosteric LH/hCG-R-agonists) can be used to restore them. The aim was to study effectiveness of separate and combined administration of metformin, hCG and 5-amino-N-tert-butyl-2-(methylsulfanyl)-4-(3-(nicotinamido)phenyl)thieno[2,3-d]pyrimidine-6-carboxamide (TP3) on steroidogenesis and spermatogenesis in male rats with T2DM. hCG (15 IU/rat/day) and TP3 (15 mg/kg/day) were injected in the last five days of five-week metformin treatment (120 mg/kg/day). Metformin improved testicular steroidogenesis and spermatogenesis and restored LH/hCG-R-expression. Compared to control, in T2DM, hCG stimulated steroidogenesis and StAR-gene expression less effectively and, after five-day administration, reduced LH/hCG-R-expression, while TP3 effects changed weaker. In co-administration of metformin and LH/hCG-R-agonists, on the first day, stimulating effects of LH/hCG-R-agonists on testosterone levels and hCG-stimulated expression of StAR- and CYP17A1-genes were increased, but on the 3–5th day, they disappeared. This was due to reduced LH/hCG-R-gene expression and increased aromatase-catalyzed estradiol production. With co-administration, LH/hCG-R-agonists did not contribute to improving spermatogenesis, induced by metformin. Thus, in T2DM, metformin and LH/hCG-R-agonists restore steroidogenesis and spermatogenesis, with metformin being more effective in restoring spermatogenesis, and their co-administration improves LH/hCG-R-agonist-stimulating testicular steroidogenesis in acute but not chronic administration.
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Herrid, Muren, Yin Xia, Tim O'Shea, and James R. McFarlane. "Leptin inhibits basal but not gonadotrophin-stimulated testosterone production in the immature mouse and sheep testis." Reproduction, Fertility and Development 20, no. 4 (2008): 519. http://dx.doi.org/10.1071/rd07062.

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The mechanisms whereby leptin regulates testosterone secretion are complex and are likely to involve actions at different levels of the hypothalamus–pituitary–gonadal axis. In the present study, the effect of leptin on testicular steroidogenesis at different developmental stages in mice and sheep was investigated. Testosterone data from testicular slice and Leydig cells of immature and adult mice testes demonstrated that the action of leptin in the regulation of steroidogenesis appears to be dependent on the developmental stage of the testis. Leptin biphasically modulates basal testosterone production in immature testicular slice cultures: at relatively low concentrations (6.25–12.5 ng mL–1) leptin exerts a significant inhibitory effect, but has less of an effect at very low (1.25 ng mL–1) or high concentrations (25 ng mL–1). However, leptin failed to modulate basal testosterone levels in Leydig cell preparations. In contrast with immature testes, leptin was unable to regulate either basal or human chorionic gonadotrophin (10 IU mL–1)-stimulated testosterone production in adult testicular slices or Leydig cell cultures. The age- and concentration-dependent regulation pattern was confirmed using sheep testicular slice culture. Leptin (1.56–25 ng mL–1) significantly inhibited basal testosterone production in the testis from birth to Day 21, but had no effect on Day 27 or older testes. However, the plasma and testicular concentrations of leptin and testosterone data in the ram indicate that such a regulatory effect of leptin on testis steroidogenesis in vitro is unable to efficiently influence testosterone concentrations in vivo. This does not exclude the possibility of a non-competitive mechanism of interaction between leptin and luteinising hormone to regulate testosterone production. Thus, we hypothesise that leptin is not an important independent regulator of testosterone concentration in the normal physiological state. The physiological significance and mechanism of leptin regulation of basal testosterone production are not known; further studies are required to elucidate these important issues.
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Santos, A. C., A. J. Conley, M. F. Oliveira, and A. C. Assis Neto. "Steroidogenesis during prenatal testicular development in Spix’s cavy Galea spixii." Reproduction, Fertility and Development 33, no. 6 (2021): 392. http://dx.doi.org/10.1071/rd20293.

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Spix’s cavy is a potentially good experimental model for research on reproductive biology and sexual development. The aim of the present study was to evaluate the ontogeny of the steroidogenic enzymes involved in testicular androgen synthesis during prenatal development. Testes were investigated on Days 25, 30, 40 and >50 of gestation. Immunohistochemistry and immunoblotting were used to establish the site and relative amount of androgenic enzymes, including 5α-reductase, cytosolic 17β-hydroxysteroid dehydrogenase (17β-HSDI) and mitochondrial microsomal 3β-hydroxysteroid dehydrogenase (3β-HSDII), throughout prenatal development. The testicular parenchyma began to organise on Day 25 of gestation, with the development of recognisable testicular cords. The mesonephros was established after Day 25 of gestation and the ducts differentiated to form the epididymis, as testicular cords were beginning to proliferate and the interstitium to organise by Day 30 of gestation, continuing thereafter. The androgen-synthesising enzymes 5α-reductase, 17β-HSDI and 3β-HSDII were evident in Leydig cells as they differentiated at all subsequent gestational ages studied. In addition, immunoblotting showed an increase in immunoreactivity for the enzymes at Days 30 and 40 of gestation (P<0.05) and a decrease at Day 50 of gestation (P<0.05). It is concluded that the increase in androgenic enzymes in Leydig cells coincides with the functional differentiation of the testes, and with the stabilisation and differentiation of mesonephric ducts forming the epididymis.
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Murphy, L., and P. J. O'Shaughnessy. "Testicular steroidogenesis in the testicular feminized (Tfm) mouse: loss of 17α-hydroxylase activity." Journal of Endocrinology 131, no. 3 (December 1991): 443–49. http://dx.doi.org/10.1677/joe.0.1310443.

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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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35

Kurt, Omer, Cenk Murat Yazici, Fetullah Gevher, Huriye Balci, Ali Yitik, and Hamdi Ozkara. "The Effect of Testicular Torsion Duration on Testicular Steroidogenesis in the Rat Model." Urologia Internationalis 97, no. 3 (2016): 358–64. http://dx.doi.org/10.1159/000443969.

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Wagner, Márcia Santos, Simone Magagnin Wajner, and Ana Luiza Maia. "The role of thyroid hormone in testicular development and function." Journal of Endocrinology 199, no. 3 (August 26, 2008): 351–65. http://dx.doi.org/10.1677/joe-08-0218.

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Thyroid hormone is a critical regulator of growth, development, and metabolism in virtually all tissues, and altered thyroid status affects many organs and systems. Although for many years testis has been regarded as a thyroid hormone unresponsive organ, it is now evident that thyroid hormone plays an important role in testicular development and function. A considerable amount of data show that thyroid hormone influences steroidogenesis as well as spermatogenesis. The involvement of tri-iodothyronine (T3) in the control of Sertoli cell proliferation and functional maturation is widely accepted, as well as its role in postnatal Leydig cell differentiation and steroidogenesis. The presence of thyroid hormone receptors in testicular cells throughout development and in adulthood implies that T3 may act directly on these cells to bring about its effects. Several recent studies have employed different methodologies and techniques in an attempt to understand the mechanisms underlying thyroid hormone effects on testicular cells. The current review aims at presenting an updated picture of the recent advances made regarding the role of thyroid hormones in male gonadal function.
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Kumar, Sudeep, Hee-Sae Park, and Keesook Lee. "Jagged1 intracellular domain modulates steroidogenesis in testicular Leydig cells." PLOS ONE 15, no. 12 (December 30, 2020): e0244553. http://dx.doi.org/10.1371/journal.pone.0244553.

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Leydig cells represent the steroidogenic lineage of mammalian testis, which produces testosterone. Genetic evidence indicates the requirement of Notch signaling in maintaining a balance between differentiated Leydig cells and their progenitors during fetal development. In primary Leydig cells, Notch1 expression decreases with testicular development, while the expression of its ligand, Jagged1, remains relatively unchanged, suggesting that the roles of Jagged1 extend beyond Notch signaling. In addition, Jagged1 is known to be processed into its intracellular domain, which then translocate to the nucleus. In this study, we investigated the effect of Jagged1 intracellular domain (JICD) on steroidogenesis in Leydig cells. The independent overexpression of JICD in MA-10 Leydig cells was found to inhibit the activity of cAMP-induced Nur77 promoter. In addition, JICD suppressed Nur77 transactivation of the promoter of steroidogenic genes such as P450scc, P450c17, StAR, and 3β-HSD. Further, adenovirus-mediated overexpression of JICD in primary Leydig cells repressed the expression of steroidogenic genes, consequently lowering testosterone production. These results collectively suggest that steroidogenesis in testicular Leydig cells, which is regulated by LH/cAMP signaling, is fine-tuned by Jagged1 during testis development.
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Gaytan, F., C. Bellido, C. Morales, M. García, N. van Rooijen, and E. Aguilar. "In vivo manipulation (depletion versus activation) of testicular macrophages: central and local effects." Journal of Endocrinology 150, no. 1 (July 1996): 57–65. http://dx.doi.org/10.1677/joe.0.1500057.

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Abstract Testicular macrophages are a relevant cell type for the regulation of Leydig cell steroidogenesis. The availability of liposome technology allows in vivo manipulation of macrophages in order to analyze their role in the regulation of the hypothalamic-pituitary-testicular axis. In this study, adult (70 days of age) and prepubertal (22 days of age) rats were injected intratesticularly with liposomes containing either dichloromethylene diphosphonate (C12MDP) to deplete testicular macrophages or muramyl tripeptide (MTP-PE) to activate them. Control rats were injected with the corresponding volumes of 0·9% NaCl. Animals were killed 10 days after treatment. Adult rats injected bilaterally or unilaterally with C12MDP liposomes showed increased serum LH and testosterone concentrations, as well as increased testosterone concentrations in the testicular interstitial fluid. In unilaterally injected rats, testosterone concentrations in the interstitial fluid were higher in the macrophage-containing testes than in the contralateral, macrophage-depleted testes. Adult rats treated bilaterally with MTP-PE liposomes showed increased numbers of testicular macrophages, whereas the number of Leydig cells was unchanged. Serum LH concentrations were decreased, but no changes were found in testosterone concentrations. Prepubertal rats treated bilaterally with C12MDP liposomes showed decreased numbers of Leydig cells. However, serum LH and testosterone concentrations were increased. Otherwise, prepubertal rats treated bilaterally with MTP-PE liposomes showed increased numbers of macrophages and Leydig cells, as well as increased serum testosterone concentrations. These data suggest that testicular macrophage-derived factors act at two different levels in the pituitary-testicular axis: first, at a central level by inhibiting LH secretion, and secondly, at a local level by stimulating Leydig cell steroidogenesis. Journal of Endocrinology (1996) 150, 57–65
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Ocón-Grove, Olga M., Susan M. Krzysik-Walker, Sreenivasa R. Maddineni, Gilbert L. Hendricks, and Ramesh Ramachandran. "NAMPT (visfatin) in the chicken testis: influence of sexual maturation on cellular localization, plasma levels and gene and protein expression." REPRODUCTION 139, no. 1 (January 2010): 217–26. http://dx.doi.org/10.1530/rep-08-0377.

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Nicotinamide phosphoribosyltransferase (NAMPT) is a cytokine hormone and rate-limiting enzyme involved in production of NAD and therefore affects a variety of cellular functions requiring NAD. Spermatogenesis and testicular steroidogenesis are likely to depend on NAD-dependent reactions and may therefore be affected by changes in testicular NAMPT expression. The objectives of the present study are to investigate testicular NAMPT expression as well as plasma NAMPT levels in prepubertal and adult chickens. By RT-PCR, NAMPT cDNA expression was detected in prepubertal and adult chicken testes. Using immunohistochemistry, NAMPT was predominantly localized in the nucleus of myoid cells, Sertoli cells, and Leydig cells in the prepubertal chicken testis. In adult chickens, however, NAMPT-immunostaining was observed in the cytoplasm of Leydig cells, Sertoli cells, primary spermatocytes, secondary spermatocytes, round spermatids, and elongated spermatids, but not in the spermatogonial cells. Using real-time quantitative PCR, adult chicken testis was found to contain fourfold greater NAMPT mRNA quantity compared with prepubertal chickens. Testicular NAMPT protein quantities determined by western blotting were not significantly different between adult and prepubertal chicken testes. Using immunoblotting, NAMPT was detected in the seminal plasma and sperm protein extracts obtained from chicken semen. Plasma NAMPT levels, determined by enzyme immunoassay, were at least 28-fold higher in the adult chickens compared with prepubertal male chickens. Taken together, sexual maturation is associated with several changes in testicular NAMPT expression indicating that NAMPT is likely to play a significant role in testicular functions such as spermatogenesis and steroidogenesis.
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Penny, Gervette M., Rebecca B. Cochran, Marjut Pihlajoki, Antti Kyrönlahti, Anja Schrade, Merja Häkkinen, Jorma Toppari, Markku Heikinheimo, and David B. Wilson. "Probing GATA factor function in mouse Leydig cells via testicular injection of adenoviral vectors." Reproduction 154, no. 4 (October 2017): 455–67. http://dx.doi.org/10.1530/rep-17-0311.

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Testicular Leydig cells produce androgens essential for proper male reproductive development and fertility. Here, we describe a new Leydig cell ablation model based on Cre/Lox recombination of mouse Gata4 and Gata6, two genes implicated in the transcriptional regulation of steroidogenesis. The testicular interstitium of adult Gata4flox/flox; Gata6flox/flox mice was injected with adenoviral vectors encoding Cre + GFP (Ad-Cre-IRES-GFP) or GFP alone (Ad-GFP). The vectors efficiently and selectively transduced Leydig cells, as evidenced by GFP reporter expression. Three days after Ad-Cre-IRES-GFP injection, expression of androgen biosynthetic genes (Hsd3b1, Cyp17a1 and Hsd17b3) was reduced, whereas expression of another Leydig cell marker, Insl3, was unchanged. Six days after Ad-Cre-IRES-GFP treatment, the testicular interstitium was devoid of Leydig cells, and there was a concomitant loss of all Leydig cell markers. Chromatin condensation, nuclear fragmentation, mitochondrial swelling, and other ultrastructural changes were evident in the degenerating Leydig cells. Liquid chromatography-tandem mass spectrometry demonstrated reduced levels of androstenedione and testosterone in testes from mice injected with Ad-Cre-IRES-GFP. Late effects of treatment included testicular atrophy, infertility and the accumulation of lymphoid cells in the testicular interstitium. We conclude that adenoviral-mediated gene delivery is an expeditious way to probe Leydig cell function in vivo. Our findings reinforce the notion that GATA factors are key regulators of steroidogenesis and testicular somatic cell survival. Free Finnish abstract: A Finnish translation of this abstract is freely available at http://www.reproduction-online.org/content/154/4/455/suppl/DC2.
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Badri, SNP, G. Vanithakumari, and T. Malini. "Studies on Methotrexate Effects on Testicular Steroidogenesis in Rats." Endocrine Research 26, no. 2 (January 2000): 247–62. http://dx.doi.org/10.3109/07435800009066165.

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42

Hwang, Eu Chang, Kyung Dai Min, Seung Il Jung, Soo Bang Ryu, Kyu Youn Ahn, Keesook Lee, and Kwangsung Park. "Testicular Steroidogenesis Is Decreased by Hyperthermia in Old Rats." Urologia Internationalis 84, no. 3 (2010): 347–52. http://dx.doi.org/10.1159/000288241.

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43

Rey, Rodolfo, Stella Campo, Sandra Ayuso, Carlos Nagle, and Héctor Chemes. "Testicular Steroidogenesis in the Cebus Monkey throughout Postnatal Development1." Biology of Reproduction 52, no. 5 (May 1, 1995): 997–1002. http://dx.doi.org/10.1095/biolreprod52.5.997.

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44

Rahman, Md Saydur, Akihiro Takemura, and Kazunori Takano. "Lunar synchronization of testicular development and steroidogenesis in rabbitfish." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 129, no. 2-3 (June 2001): 367–73. http://dx.doi.org/10.1016/s1096-4959(01)00323-2.

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45

Kwan, T. K., A. K. D. Pertiwi, N. F. Taylor, and D. B. Gower. "Steroid profiling in the study of rat testicular steroidogenesis." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 962, no. 2 (September 1988): 214–19. http://dx.doi.org/10.1016/0005-2760(88)90162-2.

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46

Tvrda, E., T. Brenkus, M. Duracka, R. Kirchner, and J. Arvay. "Anethum graveolens as a possible modulator of testicular steroidogenesis." IOP Conference Series: Earth and Environmental Science 346 (October 14, 2019): 012049. http://dx.doi.org/10.1088/1755-1315/346/1/012049.

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47

Halperin, I., and E. Vilardell. "Acute and chronic effect of ketoconazole on testicular steroidogenesis." Journal of Steroid Biochemistry 25 (January 1986): 73. http://dx.doi.org/10.1016/0022-4731(86)90660-6.

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48

Abd El-Hakim, Yasmina M., Amany Abdel-Rahman Mohamed, Safaa I. Khater, Ahmed Hamed Arisha, Mohamed M. M. Metwally, Mohamed A. Nassan, and Manal Ewaiss Hassan. "Chitosan-Stabilized Selenium Nanoparticles and Metformin Synergistically Rescue Testicular Oxidative Damage and Steroidogenesis-Related Genes Dysregulation in High-Fat Diet/Streptozotocin-Induced Diabetic Rats." Antioxidants 10, no. 1 (December 27, 2020): 17. http://dx.doi.org/10.3390/antiox10010017.

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Background: this study examined the metformin (MF) and/or chitosan stabilized selenium nanoparticles (CH-SeNPs) efficacy to alleviate the male reproductive function impairment in a high-fat diet feed with low-dose streptozotocin (HFD/STZ) induced type 2 diabetes mellitus (T2DM) diabetic rat model. Methods: control non-diabetic, HFD/STZ diabetic, HFD/STZ+MF, HFD/STZ+CH-SeNPs, and HFD/STZ+MF+CH-SeNPs rat groups were used. After 60 days, semen evaluation, hormonal assay, enzymatic antioxidant, lipid peroxidation, testis histopathology, and the steroidogenesis-related genes mRNA expressions were assessed. Results: in the HFD/STZ diabetic rats, sperm count and motility, male sexual hormones, and testicular antioxidant enzymes were significantly reduced. However, sperm abnormalities and testicular malondialdehyde were significantly incremented. The steroidogenesis-related genes, including steroidogenic acute regulatory protein (StAr), cytochrome11A1 (CYP11A1), cytochrome17A1 (CYP17A1), and hydroxysteroid 17-beta dehydrogenase 3 (HSD17B3), and the mitochondrial biogenesis related genes, including peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGCα) and sirtuin (SIRT), were significantly downregulated in the HFD/STZ diabetic rats. However, CYP19A1mRNA expression was significantly upregulated. In contrast, MF and/or CH-SeNPs oral dosing significantly rescued the T2DM-induced sperm abnormalities, reduced sperm motility, diminished sexual hormones level, testicular oxidative damage, and steroidogenesis-related genes dysregulation. In the MF and CH-SeNP co-treated group, many of the estimated parameters differ considerably from single MF or CH-SeNPs treated groups. Conclusions: the MF and CH-SeNPs combined treatment could efficiently limit the diabetic complications largely than monotherapeutic approach and they could be considered a hopeful treatment option in the T2DM.
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Petersson, Fredrik, Günter Emons, and Mats Hammar. "Testicular GnRH-Receptors and Direct Effects of a GnRH-Agonist on Human Testicular Steroidogenesis." Scandinavian Journal of Urology and Nephrology 23, no. 3 (January 1989): 161–64. http://dx.doi.org/10.3109/00365598909180835.

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50

Schuler, G., Y. Dezhkam, L. Bingsohn, B. Hoffmann, K. Failing, C. E. Galuska, M. F. Hartmann, A. Sánchez-Guijo, and S. A. Wudy. "Free and sulfated steroids secretion in postpubertal boars (Sus scrofa domestica)." REPRODUCTION 148, no. 3 (September 2014): 303–14. http://dx.doi.org/10.1530/rep-14-0193.

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Sulfated steroids have been traditionally regarded as inactive metabolites. However, they may also serve as precursors for the production of active free steroids in target cells. In this study, we used the boar as a model to study the metabolism, transport, and function of steroid sulfates due to their high production in the porcine testicular–epididymal compartment, of which the role is unknown. To characterize the secretion of free and sulfated steroids, plasma samples were collected from six postpubertal boars over 6 h every 20 min from the jugular vein. Long-term secretion profiles were also established in seven boars stimulated with human chorionic gonadotropin. To directly characterize the testicular output, samples were collected from superficial testicular arterial and venous blood vessels. Testosterone, androstenedione and sulfated pregnenolone, DHEA, estrone (E1), and estradiol-17β (E2) were determined by liquid chromatography–tandem mass spectrometry. Free E1 and E2 were measured by RIA. Irrespective of a high variability between individuals, the results suggest that i) all steroids assessed are primarily produced in the testis, ii) they exhibit similar profiles pointing to a pulsatile secretion with low frequency (three to five pulses per day), and iii) after synthesis at least a major proportion is immediately released into peripheral circulation. The fact that all steroid sulfates assessed are original testicular products and their high correlations with one another suggest their role as being intermediates of testicular steroidogenesis rather than as being inactivated end products. Moreover, a substantial use of sulfated steroids in porcine testicular steroidogenesis would assign a crucial regulatory role to steroid sulfatase, which is highly expressed in Leydig cells.
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