更新于：2024-11-01

17β-HSD3

更新于：2024-11-01

基本信息

别名

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

+ [7]

简介

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).

关联

项与 17β-HSD3 相关的药物

STX2624

靶点

17β-HSD3

作用机制

17β-HSD3 inhibitors

在研机构

Sterix Ltd.

原研机构

Sterix Ltd.

在研适应症

激素依赖性前列腺癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

RM-532-105

靶点

17β-HSD3

作用机制

17β-HSD3 inhibitors

在研机构

Université Laval

原研机构

Université Laval

在研适应症

前列腺癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

STX2171

靶点

17β-HSD3

作用机制

17β-HSD3 inhibitors

在研机构

Sterix Ltd.

原研机构

Sterix Ltd.

在研适应症

激素依赖性前列腺癌

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 17β-HSD3 相关的临床结果

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100 项与 17β-HSD3 相关的转化医学

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0 项与 17β-HSD3 相关的专利（医药）

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1,104

项与 17β-HSD3 相关的文献（医药）

2024-12-01·Toxicology Reports

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

Article

作者: 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.

2024-08-01·Environment International

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

Article

作者: 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.

2024-08-01·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

作者: 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.