Administration of Estradiol-3-Benzoate Down-Regulates the Expression of Testicular Steroidogenic Enzyme Genes for Testosterone Production in the Adult Rat.

Sakaue, Motoharu; Ishimura, Ryuta; Kurosawa, Shuhei; Fukuzawa, Noriho; Kurohmaru, Masamichi; Hayashi, Yoshihiro; Tohyama, Chiharu; Ohsako, Seiichiroh

doi:10.1292/jvms.64.107

Cited by 41 publications

(22 citation statements)

References 34 publications

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“…However, another possible explanation for our finding is that estradiol suppresses testicular CYP1B1 expression by a mechanism independent of LH. This proposal is consistent with the observation that administration of exogenous estradiol to intact adult rats leads to decreased testicular mRNA levels of steroidogenic enzymes, especially CYP17A1 and CYP11A1, but this occurs without altering serum LH levels (Sakaue et al, 2002).…”

Section: Leung Et Alsupporting

confidence: 91%

Developmental Expression and Endocrine Regulation of CYP1B1 in Rat Testis

Leung¹,

Kawai²,

Tai³

et al. 2008

Drug Metab Dispos

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ABSTRACT:Mammalian testis expresses xenobiotic-metabolizing enzymes, including cytochrome P450 1B1 (CYP1B1), which catalyzes the bioactivation of procarcinogens and other chemicals. The factors that control testicular expression of CYP1B1 are largely not known. In the present study, we investigated the influence of age and pituitary, gonadal, and thyroid hormones on CYP1B1 expression in rat testis. Immunoblot analysis showed that testicular CYP1B1 protein was expressed at a level of 5.9 ؎ 2.0 (mean ؎ S.E.M.) pmol/mg microsomal protein in prepubertal 22-day-old rats, whereas it was 6.6-fold greater in pubertal rats (34 days old) and 9.6-fold greater in adult rats (84-91 days old). Hypophysectomy decreased testicular CYP1B1 protein levels by 69% in adult rats when compared with intact rats of the same age. Intermittent subcutaneous administration of growth hormone to hypophysectomized adult rats further decreased it by 63%. Luteinizing hormone (LH) and follicle-stimulating hormone increased CYP1B1 expression in hypophysectomized rats, but they did not restore protein levels to those in intact adult male rats. Prolactin treatment alone had no effect; however, it potentiated the increase in CYP1B1 mRNA and protein expression by LH. 3,5,3-Triiodothyronine, but not thyroxine, resulted in a small increase in testicular CYP1B1 protein levels. Likewise, treatment of hypophysectomized rats with testosterone propionate elicited a small increase in CYP1B1 protein expression. In contrast, treatment of intact adult male rats with 17␤-estradiol benzoate decreased it by 91%. Overall, our findings indicate that rat testicular CYP1B1 protein expression is subject to developmental and endocrine control, with multiple hormones playing a role.

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Section: Leung Et Alsupporting

confidence: 91%

Developmental Expression and Endocrine Regulation of CYP1B1 in Rat Testis

Leung¹,

Kawai²,

Tai³

et al. 2008

Drug Metab Dispos

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“…Steroidogenic enzymes responsible for production of androgens are known to be regulated by E 2 (Sakaue et al 2002) and a decrease in testosterone levels is commonly observed with E 2 and DES administration Goyal et al 2001). The serum testosterone levels at higher doses of PPT were reduced to 25% of the control values (Fig.…”

Section: Discussionmentioning

confidence: 91%

Effect of estrogen receptor-subtype-specific ligands on fertility in adult male rats

Dumasia

Kumar

Kadam

et al. 2015

Journal of Endocrinology

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Maintenance of normal male fertility relies on the process of spermatogenesis which is under complex endocrine control by mechanisms involving gonadotropin and steroid hormones. Although testosterone is the primary sex steroid in males, estrogen is locally produced in the testis and plays a very crucial role in male fertility. This is evident from presence of both the estrogen receptors alpha (ERa) and beta (ERb) in the testis and their absence, as in the case of knockout mice models, leads to sterility. The present study was undertaken to understand individual roles of the two ERs in spermatogenesis and their direct contribution towards the maintenance of male fertility using receptor-subtype-specific ligands. Administration of ERa and b agonists to adult male rats for 60 days results in a significant decrease in fertility, mainly due to an increase in pre-and post-implantation loss and a concomitant decrease in litter size and sperm counts. Our results indicate that ERa is mainly involved in negative feedback regulation of gonadotropin hormones, whereas both ERs are involved in regulation of prolactin and testosterone production. Histological examinations of the testis reveal that ERb could be involved in the process of spermiation since many failed spermatids were observed in stages IX-XI following ERb agonist treatment. Our results indicate that overactivation of estrogen signaling through either of its receptors can have detrimental effects on the fertility parameters and that the two ERs have both overlapping and distinct roles in maintenance of male fertility.

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“…The primers used for RT-PCR for StAR protein and cytochrome P 450 scc were gene-specific primers selected according to Akingbemi et al (2004). The 3b-HSD type I and 17b-HSD type III were selected according to Sakaue et al (2002).Ten microliters of each PCR product were analyzed by gel electrophoresis on a 2% agarose gel. The molecular size of the amplified products (StAR, P450scc, 3b-HSD, 17b-HSD, and RPS 16) was determined by comparison with molecular weight marker (100 bp DNA ladder) run in parallel with RT-PCR products.…”

Section: Rt-pcrmentioning

confidence: 99%

Effects of polychlorinated biphenyl (Aroclor 1254) on steroidogenesis and antioxidant system in cultured adult rat Leydig cells

Palaniappan¹,

Balaganesh²,

Balasubramanian³

et al. 2007

Journal of Endocrinology

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Polychlorinated biphenyls (PCBs) are ubiquitous and persistent environmental contaminants that disturb normal endocrine functions, including gonadal functions in humans and mammals. In the present study, we examined the direct effects of PCB on rat Leydig cells in vitro. Adult Leydig cells were purified by Percoll gradient centrifugation method and the purity of Leydig cells was also determined by 3b-hydroxysteroid dehydrogenase (3b-HSD) staining method. Purified Leydig cells were exposed to different concentrations (10 K10-10 K7 M) of PCB (Aroclor 1254) for 24 h under basal and LH-stimulated conditions. After the experimental period, cultured media were collected and used for the assay of testosterone and estradiol. The treated cells were used for the quantification of cell-surface LH receptors and activities of steroidogenic enzymes, such as cytochrome P 450 side-chain cleavage enzyme (P 450 scc), 3b-HSD, and 17b-hydroxysteroid dehydrogenase (17b-HSD). Leydig cellular enzymatic antioxidants, such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, g-glutamyl transpeptidase, glutathione-S-transferase, and nonenzymatic antioxidants, such as vitamins C and E, were assayed. Lipid peroxidation (LPO) and reactive oxygen species (ROS) were also estimated in Leydig cells. In addition, total RNA was isolated from control and Aroclor 1254-exposed Leydig cells to monitor the steady-state mRNA levels by reverse transcription(RT)-PCR for steroidogenic acuteregulatory (StAR) protein, cytochrome P 450 scc, 3b-HSD, and 17b-HSD. Our results indicated that Aroclor 1254 (10 K9 , 10 K8 , and 10 K7 M) treatments significantly inhibit basal and LH-stimulated testosterone and estradiol production. In addition, the activities of steroidogenic enzymes, enzymatic and nonenzymatic antioxidants were significantly diminished in a dose-dependent manner. However, LPO and ROS were elevated in a dose-dependent manner under basal and LH-stimulated conditions. RT-PCR analysis of StAR mRNA level showed a decrease only in 10 K7 M dose of Aroclor 1254 treatment, while cytochrome P 450 scc, 3b-HSD, and 17b-HSD mRNAs were drastically decreased in both 10 K8 and 10 K7 M Aroclor 1254 treatment. These findings suggest that PCBs can act directly on Leydig cells to diminish testosterone production by inhibiting gene expression of steroidogenic enzymes and antioxidant system.

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Administration of Estradiol-3-Benzoate Down-Regulates the Expression of Testicular Steroidogenic Enzyme Genes for Testosterone Production in the Adult Rat.

Cited by 41 publications

References 34 publications

Developmental Expression and Endocrine Regulation of CYP1B1 in Rat Testis

Developmental Expression and Endocrine Regulation of CYP1B1 in Rat Testis

Effect of estrogen receptor-subtype-specific ligands on fertility in adult male rats

Effects of polychlorinated biphenyl (Aroclor 1254) on steroidogenesis and antioxidant system in cultured adult rat Leydig cells

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