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Adrenocortical carcinoma
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Dushyanthy Arasaratnam, Nadia Barghouthi, Vladimer Bakhutashvili
Individual steroid metabolite profiles can also be used to monitor for recurrence, progression, and treatment response.6 Plasma 17-hydroxysteroids, corticosterone, deoxycortisol, and cortisone can all rise during pregnancy, mirroring the 2- to 3-fold rise of cortisol.9 This makes the use of these steroid precursors challenging, as normative data ranges for pregnancy have not been established.
Role of Steroids in the Onset of Labor
Published in Robert E. Garfield, Thomas N. Tabb, Control of Uterine Contractility, 2019
Guy Germain, Leroy Marie Josèphe, Michelle Breuiller-Fouche
Experimental modulation of the influence exerted by progesterone on target tissues during late pregnancy has been achieved by several means: (1) overload of the natural hormone or administration of synthetic analogs; (2) ovariectomy, which is relevant only in species that depend on some degree to ovarian support during the entire gestation; (3) fetectomies, which disrupt in primates the fetus-driven synthesis of estrogens; (4) inhibition of progesterone secretion by competitive inhibitors of 3β-hydroxysteroid dehydrogenase; (5) administration of progesterone antagonists acting at the level of the hormone receptor.
Hormones
Published in S.J. Mulé, Henry Brill, Chemical and Biological Aspects of Drug Dependence, 2019
The chronic administration of morphine to iats produces a marked adrenal cortical hypertrophy. This observation, first made in 1926 by McKay and McKay,21 has since been confirmed by others.22–25 Investigations in which different parameters of pituitary-adrenal activity were studied seem to indicate an opposite effect, i.e., chronic administration of morphine depresses the basal level of adrenal cortical secretion. The injection of morphine into guinea pigs for 12 days was found to reduce the basal level of urinary 17-hydroxysteroids.17 Similar findings have been observed in the rat and in man. Paroli and Melchiorri26 injected rats for periods ranging between 10 to 40 days and 40 to 100 days and noted a decrease in the urinary levels of hydroxysteroids. In a study on human addicts Eisenman et al.27 found that two-to-four month cycles of morphine addiction reduced both plasma and urinary 17-hydroxycorticosteroid levels. They showed that this reduction in the basal secretory rate of adrenal cortical hormones was due chiefly to a decrease in production of 17-OHCS, rather than an increase in their degradation. Furthermore, this reduction was not the result of the adrenal cortex becoming insensitive to ACTH, since the injection of ACTH during the addiction cycles produced an increase in 17-OHCS which was comparable to the response obtained during the preaddic-tion period.
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.
Deciding on the appropriate pharmacotherapy for the treatment of endometriosis
Published in Expert Opinion on Pharmacotherapy, 2023
As we gain more knowledge on the pathological cascade leading to endometriosis, the possibility of identifying specific agents which could block essential pathways and prevent disease progression and development increases. Promising results may be on the horizon with the novel 17-β-hydroxysteroid dehydrogenase (HSD17B) inhibitors (Forendo Pharma’s FOR-6219) which exert local action blocking the conversion of the weak estrone into the potent estradiol. Thus, local estrogen production remains low without affecting systemic levels, resulting in inhibition of lesion development and progression, as well as decreased endometrial cell proliferation and inflammation. The major advantage would be the reduction of systemic effects with greater tolerability. Clinical tests should be starting soon [28]. Noncoding RNAs have been identified as key players in various diseases including endometriosis and several microRNA are involved in cell migration and proliferation and may represent a target for drug development.
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.