PERINATAL HORMONE LEVELS AND THEIR ROLE IN NORMAL/ABNORMAL DEVELOPMENT AND FUNCTION OF THE MALE REPRODUCTIVE SYSTEM

1999 ◽  
Vol 27 (1) ◽  
pp. A5-A5
Author(s):  
R. Sharpe
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 ◽  
...  

2019 ◽  
Vol 87 ◽  
pp. 146-155 ◽  
Author(s):  
Birce Sunman ◽  
Kadriye Yurdakök ◽  
Belma Kocer-Gumusel ◽  
Özgür Özyüncü ◽  
Filiz Akbıyık ◽  
...  

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.


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