Last update 01 Nov 2024

17β-HSD3

Last update 01 Nov 2024

Basic Info

Synonyms

17-beta-HSD 3, 17-beta-hydroxysteroid dehydrogenase type 3, EDH17B3

+ [7]

Introduction

Catalyzes the conversion of 17-oxosteroids to 17beta-hydroxysteroids (PubMed:8075637, PubMed:16216911, PubMed:27927697, PubMed:26545797). Favors the reduction of androstenedione to testosterone (PubMed:16216911, PubMed:27927697, PubMed:26545797). Testosterone is the key androgen driving male development and function (PubMed:8075637). Uses NADPH while the two other EDH17B enzymes use NADH (PubMed:26545797, PubMed:8075637, PubMed:16216911). Androgens such as epiandrosterone, dehydroepiandrosterone, androsterone and androstanedione are accepted as substrates and reduced at C-17 (PubMed:16216911). Can reduce 11-ketoandrostenedione as well as 11beta-hydroxyandrostenedione at C-17 to the respective testosterone forms (PubMed:16216911, PubMed:27927697).

Drugs associated with 17β-HSD3

STX2624

Target

17β-HSD3

Mechanism

17β-HSD3 inhibitors

Active Org.

Sterix Ltd.

Originator Org.

Sterix Ltd.

Active Indication

Hormone-dependent prostate cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

RM-532-105

Target

17β-HSD3

Mechanism

17β-HSD3 inhibitors

Active Org.

Université Laval

Originator Org.

Université Laval

Active Indication

Prostatic Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

STX2171

Target

17β-HSD3

Mechanism

17β-HSD3 inhibitors

Active Org.

Sterix Ltd.

Originator Org.

Sterix Ltd.

Active Indication

Hormone-dependent prostate cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with 17β-HSD3

100 Translational Medicine associated with 17β-HSD3

0 Patents (Medical) associated with 17β-HSD3

1,104

Literatures (Medical) associated with 17β-HSD3

01 Dec 2024·Toxicology Reports

Ameliorative action of eugenol on nitrate induced reproductive toxicity in male rats

Article

Author: Sarjan, Halugudde Nagaraja ; Shivabasavaiah ; Rajini, Sulanaikanahalli Vadyappa

There is a great concern for studies to prevent nitrate (NO₃) induced male reproductive toxicity as it might lead to infertility. Therefore, the study was aimed to investigate the ameliorative effects of eugenol on NO₃ induced male reproductive toxicity in wistar rats. Adult male rats were randomly divided into five groups (n=5). The first group was served as control, the second and third group of rats were treated with 100 mg/kg bw of sodium nitrate (NaNO₃) and NO₃ contaminated ground water respectively. The fourth and fifth group of rats were orally intubated with eugenol (100 mg/kg bw) and then exposed to NaNO₃ and NO₃ contaminated ground water respectively. The treatment was continued for 52 days. Nitrate exposure significantly decreased the sperm motility, testicular 3-beta-hydroxysteroid dehydrogenase activity, serum concentration of testosterone, activities of superoxide dismutase and catalase in testis and spermatozoa and different categories of germ cells in stage VII of spermatogenesis. Further, there was significant increase in sperm abnormality and levels of nitrite (NO₂) and malondialdehyde in testis and spermatozoa of NO₃ treated rats. In addition, NO₃ exposure distorted the histological architecture of seminiferous tubules of testis. It was established that NO₃ induced high production of NO₂ affected spermatogenesis, steroidogenesis and sperm motility. However, in the present study, pretreatment of eugenol prevented NO₃ induced reproductive alterations by decreasing the level of NO₂. These findings clearly showed the protective action of eugenol against NO₃ induced oxidative stress in male reproductive system.

01 Aug 2024·Environment International

Triclosan inhibits testosterone biosynthesis in adult rats via inducing m6A methylation-mediated autophagy

Article

Author: Yan, Jingyun ; Wang, Hong ; Quan, Hehua ; Mao, Zhixiang ; Ge, Ren-Shan ; Lin, Han ; Ji, Zhongyao ; Li, Huitao ; Sang, Jianmin ; Yu, Yang ; Li, Linxi ; Wang, Yiyan

Triclosan is a potent antibacterial compound widely used in everyday products. Whether triclosan affects Leydig cell function in adult male rats remains unknown. In this study, 0, 50, 100, or 200 mg/kg/day triclosan was gavaged to Sprague-Dawley male rats from 56 to 63 days postpartum. Triclosan significantly reduced serum testosterone levels at ≥ 50 mg/kg/day via downregulating the expression of Leydig cell gene Lhcgr, Scarb1, Star, Cyp11a1, Hsd3b1, Cyp17a1, and Hsd17b3 and regulatory transcription factor Nr3c2 at 100-200 mg/kg. Further analysis showed that triclosan markedly increased autophagy as shown by increasing LC3II and BECN1 and decreasing SQSTM1. The mRNA m6A modification analysis revealed that triclosan significantly downregulated Fto expression at 200 mg/kg while upregulating Ythdf1 expression at 100 and 200 mg/kg, leading to methylation of Becn1 mRNA as shown by MeRIP assay. Triclosan significantly inhibited testosterone output in rat R2C Leydig cells at ≥ 5 μM via downregulating Fto and upregulating Ythdf1. SiRNA Ythdf1 knockdown can reverse triclosan-mediated mitophagy in R2C cells, thereby reversing the reduction of testosterone output. In summary, triclosan caused Becn1 m6A methylation by downregulating Fto and upregulating Ythdf1, which accelerated Becn1 translation, thus leading to the occurrence of autophagy and the decrease of testosterone biosynthesis.

01 Aug 2024·Aquatic Toxicology

The impact of co-exposure to polystyrene microplastics and norethindrone on gill histology, antioxidant capacity, reproductive system, and gut microbiota in zebrafish (Danio rerio)

Article

Author: Hou, Liping ; Lin, Zhong ; Liang, Yan-Qiu ; Li, Chengyong ; Lin, Hongjie ; Pan, Chang-Gui ; Dong, Zhongdian ; Lian, Xiaoyi ; Zhou, Shuhui ; Liu, Ziyun

In recent years, studies have focused on the combined ecological risks posed by microplastics and other organic pollutants. Although both microplastics and progestin residues are frequently detected in the aquatic environments, their ecological implications remain unknown. Adult zebrafish were exposed to polystyrene microplastics (PS, 200 nm, 200 μg/L), norethindrone (NET, 69.6 ng/L), and their mixture (200 μg/L PS + 63.1 ng/L NET) for 30 days. The results demonstrated that exposure to PS and NET resulted in gill damage. Notably, the PS and PS+NET exhibited a significant decrease in glutathione (GSH) and oxidized glutathione (GSSG) content, as well as reduced antioxidase activity in the gills. The oxidative stress in PS+NET primarily originated from PS. The PS, NET, or their mixture resulted in a decrease in testosterone (T) and estradiol (E2) levels in female. Furthermore, compared to NET, the PS+NET showed a significant reduction in E2 levels, thereby augmenting the inhibitory effect on reproductive ability mediated by NET. However, males showed an increase in 11-ketodihydrotestosterone (11-KT) content, accompanied by a significant decrease in spermatogonia (Sg) and increase in spermatocytes (Sc). Consequently, it can be inferred that PS enhances the androgenic effect of NET. In female fish brain, NET alone resulted in transcriptional down-regulation of partial hormone receptors; however, co-administration of PS effectively mitigated the interference effects. Furthermore, transcriptional downregulation of 17-alpha-hydroxylase (cyp17), hydroxysteroid 3-beta dehydrogenase (hsd3b), estrogen receptor 1 (esr1), and estrogen receptor 2a (esr2b) genes in the ovary was found to be associated with the androgenic activity induced by NET. Moreover, in comparison to PS or NET alone, PS+NET resulted in a notable decrease in Cetobacterium abundance and an increase in Aeromonas population, suggesting that the co-exposure of PS+NET may exacerbate intestinal burden. The findings highlight the importance of studying the combined toxicity of PS and NET.

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17β-HSD3

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