Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Estrogenic endocrine disruptor exposure directly impacts erectile function.
Commun Biol
April 2024
School of BioSciences, The University of Melbourne, Melbourne, Australia.
Article Synopsis
- Erectile dysfunction (ED) is a common condition that adversely affects quality of life, and its rising prevalence suggests potential environmental risk factors.
- The study investigates the impact of Endocrine Disrupting Chemicals (EDCs), particularly diethylstilbestrol (DES), on erectile function by using male mice as a model.
- Findings reveal that chronic exposure to DES leads to abnormal erectile tissue function and increased expression of estrogen receptors, indicating that both long-term and short-term exposure to estrogenic EDCs may play a significant role in causing ED.
The Possible Role of Prescribing Medications, Including Central Nervous System Drugs, in Contributing to Male-Factor Infertility (MFI): Assessment of the Food and Drug Administration (FDA) Pharmacovigilance Database.
Brain Sci
November 2023
ASST Sette Laghi-Circolo e Fondazione Macchi Hospital, 21100 Varese, Italy.
Article Synopsis
- A study investigated the relationship between various medications and male-factor infertility (MFI), identifying a range of drugs potentially linked to the condition through a thorough review of the FDA's adverse event reporting database.
- Out of 955 MFI reports analyzed, 408 were associated with 20 specific medications, with notable findings on finasteride, testosterone, and diethylstilbestrol showing significantly high reporting ratios.
- The research concluded that while many medications already suspected of contributing to MFI were confirmed, some hypothesized agents were not represented, suggesting a need for further investigation in pharmacovigilance.
Chemicals of environmental concern as inhibitors of human placental 3β-hydroxysteroid dehydrogenase 1 and aromatase: Screening and docking analysis.
Chem Biol Interact
December 2022
Department of Emergency Medicine, The Second Affiliated Hospital and Yuying Children Hospital of Wenzhou Medical University, Zhejiang, 325000, PR China; Department of Obstetrics and Gynecology, The Second Affiliated Hospital and Yuying Children Hospital of Wenzhou Medical University, Zhejiang, 325000, PR China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325000, Zhejiang Province, PR China. Electronic address:
Many environmental pollutants act as endocrine-disrupting compounds by inhibiting human placental 3β-hydroxysteroid dehydrogenase/Δ isomerase type 1 (HSD3B1) and aromatase (CYP19A1) activities. In this study, we screened 13 chemicals of environmental concern for their ability to inhibit human HSD3B1 and CYP19A1 by measuring the conversion of pregnenolone to progesterone for HSD3B1 activity and the conversion of testosterone to 17β-estradiol for CYP19A1 activity in human JEG-3 choriocarcinoma cell microsomes. HSD3B1 had an apparent Km of 0.
View Article and Find Full Text PDFMaintaining bone health by estrogen therapy in patients with advanced prostate cancer: a narrative review.
Endocr Connect
December 2022
Andros Clinics, Arnhem, The Netherlands.
The purpose of androgen deprivation therapy (ADT) in prostate cancer (PCa), using luteinizing hormone-releasing hormone agonists (LHRHa) or gonadotrophin-releasing hormone antagonists, is to suppress the levels of testosterone. Since testosterone is the precursor of estradiol (E2), one of the major undesired effects of ADT is the concomitant loss of E2, causing among others an increased bone turnover and bone loss and an increased risk of osteoporosis and fractures. Therefore, the guidelines for ADT indicate to combine ADT routinely with bone-sparing agents such as bisphosphonates, denosumab or selective estrogen receptor modulators.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!