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Ethnomedicinal and Pharmacological Importance of Glycyrrhiza glabra L
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Ashish K. Bhattarai, Sanjaya M. Dixit
High intake of licorice can cause hyper mineralocorticoidism with sodium retention and potassium loss, oedema, increased blood pressure, and depression of the renin-angiotensin-aldosterone system. As a result, the number of related clinical symptoms are reported. There is increased cortisol level in the kidneys and other mineralocorticoid selective tissues because of the inhibition of enzymes involved in the metabolism of corticosteroids. Glycyrrhetic acid inhibits the enzyme 11β-hydroxysteroid dehydrogenase involved in the metabolism of corticosteroids which is produced after glycyrrhizic acid is hydrolyzed in the intestine. This cortisol results in hyper mineralocorticoid effect. The compensatory physiological mechanisms following hyper mineralocorticoids, which is depression of the renin-angiotensin system, can last several months. The inhibitory effect on 11β-hydroxysteroid dehydrogenase is reversible. So after the withdrawal of consumption of licorice, there is physiological reversal of hyper mineralocorticoids, but it takes several months (Størmer et al. 1993).
Overview of Perinatal Maternal Stress
Published in Rosa Maria Quatraro, Pietro Grussu, Handbook of Perinatal Clinical Psychology, 2020
Dawn Kingston, Muhammad Kashif Mughal
Third, 11β-HSD2 is the gene responsible for cortisol regulation in the placenta. It codes for production of the enzyme, 11-β-hydroxysteroid dehydrogenase, which metabolizes active cortisol into inactive cortisone. Methylation of this gene has been associated with sub-optimal neurobehavioral outcomes and increased cortisol in infants (Cao-Lei et al., 2017). Another study showed that infants of women who were psychologically distressed during pregnancy had greater 11β-HSD2 methylation than infants of mothers who were not distressed, and this was associated with infant hypotonia (Conradt et al., 2013).
Environmental toxicants on Leydig cell function
Published in C. Yan Cheng, Spermatogenesis, 2018
Leping Ye, Xiaoheng Li, Xiaomin Chen, Qingquan Lian, Ren-Shan Ge
There are 14 different 17β-hydroxysteroid dehydrogenase isoforms.25 Different isoforms of 17β-HSD are encoded by different genes. The only isoform involved in testosterone production in Leydig cells is 17β-hydroxysteroid dehydrogenase isoform 3 (17β-HSD3), which is encoded by human HSD17B336 or rat Hsd17b3.16
Curcumin analogues exert potent inhibition on human and rat gonadal 3β-hydroxysteroid dehydrogenases as potential therapeutic agents: structure-activity relationship and in silico docking
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Xinyi Qiao, Lei Ye, Jialin Lu, Chengshuang Pan, Qianjin Fei, Yang Zhu, Huitao Li, Han Lin, Ren-shan Ge, Yiyan Wang
Adrenal and gonadal 3β-hydroxysteroid dehydrogenase/Δ5,4-isomerases (3β-HSDs) are hydroxysteroid dehydrogenase subfamily members that play critical role in the second step catalysis for adrenal glucocorticoid and mineralocorticoid and gonadal sex steroid biosynthesis. They catalyse the conversion from pregnenolone (P5) or dehydroepiandrosterone (DHEA) to progesterone (P4) or androstenedione (Figure 1(B)), which are precursors of potent glucocorticoids, mineralocorticoids, androgens, and oestrogens9. Two isoforms of 3β-HSD have been cloned in humans, type 1 3β-HSD1 (h3β-HSD1) and type 2 (h3β-HSD2), and h3β-HSD2 is exclusively present in adrenals and gonads for its function. In the rat model, 4 isoforms have been cloned, rat type 1 (r3β-HSD1) is primarily present in gonadal cells (including testicular Leydig cells)9.
Trophectoderm non-coding RNAs reflect the higher metabolic and more invasive properties of young maternal age blastocysts
Published in Systems Biology in Reproductive Medicine, 2023
Panagiotis Ntostis, Grace Swanson, Georgia Kokkali, David Iles, John Huntriss, Agni Pantou, Maria Tzetis, Konstantinos Pantos, Helen M. Picton, Stephen A. Krawetz, David Miller
LncRNAs of enzymes reported in the current study, are involved in cholesterol biosynthesis and/or steroidogenesis. Hydroxysteroid dehydrogenases along with the steroidogenic acute regulatory (STAR) and START-domain proteins play important roles in steroidogenesis (Ye et al. 2021), with the lipid-binding STARD4 participating in cholesterol intracellular transport, playing important roles in cellular metabolism. The high expression levels of these lncRNAs in the YMA/rba-YMA group along with the increased corresponding mRNA levels, suggests that the first may act either by enhancing the expression of the latter or inhibit the sncRNAs that regulate their mRNAs, with the same outcome. The current study reported that MGST1 lncRNA was approximately 5 times more highly expressed in the YMA/rba-YMA than in the AMA/rba-AMA trophectoderm group. MGST1 is a glutathione transferase involved in cellular metabolism, stem cell development and differentiation and when absent is embryonic lethal (Bräutigam et al. 2018), perhaps by affecting blastocyst differentiation and/or stem cell differentiation during embryo development. The HSD17B1 lncRNA, participating in cholesterol synthesis/steroidogenesis that is important for early embryo development, was expressed approximately 10 times more highly in YMA/rba-YMA blastocysts than AMA/rba-AMA blastocysts. This lncRNA was associated with blastocysts showing higher implantation success rates potentially enhancing the expression of HSD17B1 (Ntostis et al. 2015; Ntostis et al. 2019; Ntostis et al. 2021).
Antioxidant and anti-inflammatory protective effects of rutin and kolaviron against busulfan-induced testicular injuries in rats
Published in Systems Biology in Reproductive Medicine, 2022
Sunny O. Abarikwu, Rex-Clovis C. Njoku, Ifeoma G. John, Benjamin A. Amadi, Chidimma J. Mgbudom-Okah, Chigozie L. Onuah
3β-hydroxysteroid dehydrogenase is a key enzyme in the biosynthesis of all active steroid hormones, and it exerts a regulatory control on the testicular steroid hormone cascade system (Abarikwu et al. 2014; Alamdar et al. 2017). It is believed that the activity of 3β-HSD in the testis is essential for normal steroidogenesis and subsequently for the reproductive capacity of most mammalian animal species (Rasmussen et al. 2013). The finding that 3β-HSD activity was increased in the BUS-treated animals in the present study is consistent with our previous study, and thought to be a compensatory attempt by the testes to drive androgen synthesis (Abarikwu et al. 2020). Interestingly, rutin and kolaviron co-treatment alone or in combination decreased 3β-HSD activity. However, rutin co-treatment (BUS + RUT) had better protective effects on 3β-HSD activity than when kolaviron and rutin were combined (BUS + KV + RUT) or when kolaviron was administered separately (BUS + KV). It may appear that kolaviron and rutin did not exhibit a strong protective effect on 3β-HSD activity in the rat’s testes as a result of the antagonism of both phenolics (Phan et al. 2018b). Considering that these phenolics occur in nature and prevalently in combinations in seeds and fruits, giving them together might not amplify their efficacy against busulfan-induced disturbances in androgen production in animals and clinical models.