scholarly journals Antiandrogenic and Estrogenic Compounds: Effect on Development and Function of Male Reproductive System

Author(s):  
Anna Hejmej ◽  
Magorzata Kotula-Balak ◽  
Barbara Bilinsk
Endocrinology ◽  
2008 ◽  
Vol 149 (8) ◽  
pp. 4209-4217 ◽  
Author(s):  
Brenda Anguiano ◽  
Nuri Aranda ◽  
Guadalupe Delgado ◽  
Carmen Aceves

We characterized the enzymes that catalyze the deiodination of T4 to T3 in the male reproductive tract. Testis, epididymis (EPI), seminal vesicles, prostate, bulbourethral glands, spermatozoa, and semen were taken from sexually mature rats (300 g). Iodothyronine 5′-deiodinase (5′-D) activity was quantified by the radiolabeled-iodide-release method. 5′-D activity was 10-fold higher in EPI and semen than in the rest of the tissues. In EPI, semen, and prostate, the enzymatic activity was completely inhibited by 1 mm 6-n-propyl-2-thiouracil, whereas in the other tissues the inhibition was partial (50%). The high susceptibility to 6-n-propyl-2-thiouracil inhibition, a ping-pong kinetic pattern, and low cofactor (Michaelis Menten constant for dithiothreitol = 0.7 mm) and high substrate (Michaelis Menten constant for reverse T3 = 0.4 μm) requirements indicate that EPI 5′-D corresponds to type 1 deiodinase (D1). Real-time RT-PCR amplification of D1 mRNA in this tissue confirms this conclusion. The highest EPI D1 expression occurred at the onset of puberty and sexual maturity, and in the adult, this activity was more abundant in corpus and caput than in the caudal region. EPI D1 expression was elevated under conditions of hyperthyroidism and with addition of 17β-estradiol. Our data also showed a direct association between D1 and a functional epididymis marker, the neutral α-glucosidase enzyme, suggesting that local generation of T3 could be associated with the development and function of EPI and/or spermatozoa maturation. Further studies are necessary to analyze the possible physiological relevance of 5′-D in the male reproductive system.


2009 ◽  
Vol 53 (8) ◽  
pp. 923-933 ◽  
Author(s):  
Maria Fatima Magalhães Lazari ◽  
Thais Fabiana Gameiro Lucas ◽  
Fabiana Yasuhara ◽  
Gisele Renata Oliveira Gomes ◽  
Erica Rosanna Siu ◽  
...  

A substantial advance in our understanding on the estrogen signaling occurred in the last decade. Estrogens interact with two receptors, ESR1 and ESR2, also known as ERα and ERβ, respectively. ESR1 and ESR2 belong to the nuclear receptor family of transcription factors. In addition to the well established transcriptional effects, estrogens can mediate rapid signaling, triggered within seconds or minutes. These rapid effects can be mediated by ESRs or the G protein-coupled estrogen receptor GPER, also known as GPR30. The effects of estrogen on cell proliferation, differentiation and apoptosis are often mediated by growth factors. The understanding of the cross-talk between androgen, estrogen and growth factors signaling pathways is therefore essential to understand the physiopathological mechanisms of estrogen action. In this review we focused on recent discoveries about the nature of the estrogen receptors, and on the signaling and function of estrogen in the male reproductive system.


2019 ◽  
Vol 280 (11) ◽  
pp. 1693-1705
Author(s):  
Luis M. Pardo ◽  
Fernando J. Zara ◽  
Marcela P. Riveros ◽  
Kurt Paschke ◽  
Katrin Pretterebner ◽  
...  

2017 ◽  
Author(s):  
Dianrong Li ◽  
Lingjun Meng ◽  
Tao Xu ◽  
Yaning Su ◽  
Xiao Liu ◽  
...  

AbstractNecroptosis is a form of programmed necrotic cell death in mammals that is mediated by a pair of kinases, RIP1 and RIP3, as well as the RIP3 substrate MLKL. We report here that male reproductive organs of both RIP3-and MLKL-knockout mice retain “youthful” morphology and function into advanced age, while those of age-matched wild type mice deteriorate. The RIP3 phosphorylation of MLKL, the activation marker of necroptosis, is detected in spermatogonial stem cells in the testes of old but not in young wild type mice. When the testes of young wild type mice are given a local necroptotic stimulus, their reproductive organs showed accelerated aging. Feeding of wild type mice with an RIP1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging. Thus, necroptosis in testes promotes the aging-associated deterioration of the male reproductive system in mice.


eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Dianrong Li ◽  
Lingjun Meng ◽  
Tao Xu ◽  
Yaning Su ◽  
Xiao Liu ◽  
...  

A pair of kinases, RIPK1 and RIPK3, as well as the RIPK3 substrate MLKL cause a form of programmed necrotic cell death in mammals termed necroptosis. We report here that male reproductive organs of both Ripk3- and Mlkl-knockout mice retain ‘youthful’ morphology and function into advanced age, while those of age-matched wild-type mice deteriorate. The RIPK3 phosphorylation of MLKL, the activation marker of necroptosis, is detected in spermatogonial stem cells in the testes of old but not in young wild-type mice. When the testes of young wild-type mice are given a local necroptotic stimulus, their reproductive organs showed accelerated aging. Feeding of wild-type mice with an RIPK1 inhibitor prior to the normal onset of age-related changes in their reproductive organs blocked the appearance of signs of aging. Thus, necroptosis in testes promotes the aging-associated deterioration of the male reproductive system in mice.


2021 ◽  
Author(s):  
Fanli Sun ◽  
Xuying Wang ◽  
Pinzheng Zhang ◽  
Ziyun Chen ◽  
Zhiyi Guo ◽  
...  

Abstract BackgroundPuberty is a crucial stage to gain reproductive capacity, but it is also a period vulnerable to exogenous materials. While exposure to nanoparticles (NPs) has been linked to toxic responses in reproductive system in previous findings, little is known about the age-dependent effect of NPs, let alone the underlying mechanism. In the present study, we assessed male fertility parameters and explored its mechanism following intraperitoneal exposure to Nano-Silicon dioxide (Nano-SiO2) in mice during puberty.Methods40 mice aged 5 weeks were divided into 2 groups after 1 week acclimation and then exposed to 40mg/kg Nano-SiO2 dissolved in saline or vehicle controls by intraperitoneal injection every day over a period of 7-day, respectively. Changes in the structure and function of male reproductive organs were detected after exposure.ResultsNano-SiO2 exposed through intraperitoneal injection could cause damage to the testicular and epididymal histological architecture and reduce the level of sex hormone (testosterone), leading to a decrease in sperm quality and quantity. Furthermore, Nano-SiO2 could induce oxidative stress and inflammation in male reproductive tissues, indicated by reduced activity of antioxidants (superoxide dismutase, SOD) and increased level of the lipid peroxidation marker (malondialdehyde, MDA), which leads to the activation of cell apoptosis.ConclusionExposure to Nano-SiO2 in pubertal mice could cause toxicity on male reproductive system via inducing oxidative stress and activating TNF-α mediated apoptotic pathway.


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