Human sperm anatomy and endocrinology in varicocele: role of androgen receptor

Guido, Carmela; Santoro, Marta; Amicis, Francesca De; Perrotta, Ida; Panza, Salvatore; Rago, Vittoria; Cesario, Maria Grazia; Lanzino, Marilena; Aquila, Saveria

doi:10.1530/rep-13-0542

Cited by 19 publications

(11 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Reduced androgen receptor (AR) expression was evident in the spermatozoa of varicocele patients with respect to spermatozoa from fertile men; and dihydrotestosterone (DHT) treatment increased the cholesterol influx in normal sperm but had little effect on spermatozoa of varicocele patients (Guido et al, 2014). This finding may indicate that reduced AR expression in the spermatozoa of varicocele patients can contribute to the difficulty experienced in switching to a capacitated status (Guido et al, 2014).…”

Section: Decreased Androgen Receptor Expression In Spermatozoa Of Submentioning

confidence: 99%

A global view of the pathophysiology of varicocele

2018

View full text Add to dashboard Cite

Varicocele is the most common abnormality identified in men being evaluated for subfertility. In this comprehensive review of the pathophysiology of varicocele, we will shed light on novel pathophysiological findings and their clinical implications that may direct future researches; we will shed light on the impact of transient scrotal hyperthermia and the roles of inflammation and differential protein expression and androgen expression in spermatozoa on inducing pathophysiological findings. Furthermore, we will clarify the linked processes contributing to the pathophysiology of varicocele and the impact of genetics on the induction of these processes. Spermatogenesis is a temperature-sensitive process, and heat stress of varicocele is considered the most plausible cause of impaired spermatogenesis. The three processes associated with the presence of varicocele - heat stress, excess reactive oxygen species, and increased apoptosis - appear to be linked; heat stress is associated with increased levels of reactive oxygen species and oxidative stress, which can induce apoptosis. The genetic role should not be overlooked as a contributing factor in the induction of heat stress, excess reactive oxygen species/oxidative stress, and apoptosis; this is evidenced by the association of varicocele with decreased expression of heat-shock proteins, higher polymorphism of glutathione S transferase and nitric oxide synthase genes, and increased BAX and decreased BCL2 genes and proteins. In this article, we will highlight the need of application of novel diagnostic techniques that can provide a precise pathophysiological diagnosis to guide potential specific innovative therapies. Innovative therapies can counteract the varicocele-induced stasis, suppress the degenerative effects of testicular hyperthermia, reduce the varicocele-induced apoptosis, and target the elevated-neutrophil products aiming at abrogating the testicular damage caused by the induced varicocele in rats/mice. In conclusion, on the basis of the novel scientific research, it may be possible to formulate new treatments and achieve the appropriate selection of patients who can benefit from these treatments.

show abstract

Section: Decreased Androgen Receptor Expression In Spermatozoa Of Submentioning

confidence: 99%

A global view of the pathophysiology of varicocele

2018

View full text Add to dashboard Cite

show abstract

“…In addition, varicocele has long been known to have an adverse impact on fertility and sex hormone production, and while the mechanism of this affect is unknown, estrogen has been linked. 55 56 Semen analysis of “varicocele” sperm showed a marked reduction in both ER alpha and beta receptors as well as a reduced response to estradiol's necessary effects on motility and acrosin activity. 56 …”

Section: Role Of Estradiol In Spermatogenesismentioning

confidence: 99%

The role of estradiol in male reproductive function

2016

View full text Add to dashboard Cite

Traditionally, testosterone and estrogen have been considered to be male and female sex hormones, respectively. However, estradiol, the predominant form of estrogen, also plays a critical role in male sexual function. Estradiol in men is essential for modulating libido, erectile function, and spermatogenesis. Estrogen receptors, as well as aromatase, the enzyme that converts testosterone to estrogen, are abundant in brain, penis, and testis, organs important for sexual function. In the brain, estradiol synthesis is increased in areas related to sexual arousal. In addition, in the penis, estrogen receptors are found throughout the corpus cavernosum with high concentration around neurovascular bundles. Low testosterone and elevated estrogen increase the incidence of erectile dysfunction independently of one another. In the testes, spermatogenesis is modulated at every level by estrogen, starting with the hypothalamus-pituitary-gonadal axis, followed by the Leydig, Sertoli, and germ cells, and finishing with the ductal epithelium, epididymis, and mature sperm. Regulation of testicular cells by estradiol shows both an inhibitory and a stimulatory influence, indicating an intricate symphony of dose-dependent and temporally sensitive modulation. Our goal in this review is to elucidate the overall contribution of estradiol to male sexual function by looking at the hormone's effects on erectile function, spermatogenesis, and libido.

show abstract

“…Androgens have an important role in spermatogenesis and male infertility [ 30 ]. Testosterone androgen is essential for spermatogenesis and secondary sexual characteristic expression [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

The expression of cyclic adenosine monophosphate responsive element modulator in rat sertoli cells following seminal extract administration

et al. 2016

View full text Add to dashboard Cite

Aim:This study aims to determine the effect of seminal vesicle extract on cyclic adenosine monophosphate responsive element modulator (CREM) expression in rat Sertoli cells.Materials and Methods:This study examined the expression of CREM on 20 male rats (Rattus norvegicus) at 4 months of age, weighing 250-300 g. The rats were divided into four groups: K0, KP1, KP2, and KP3. K0 group was injected with 0.2 ml normal saline; KP1 was injected with 25 mg cloprostenol (Prostavet C, Virbac S. A); KP2 and KP3 were injected with 0.2 and 0.4 ml seminal vesicle extract, respectively. The treatments were conducted 5 times within 12-day interval. At the end of the study, the rats were euthanized by cervical dislocation; then, the testicles were necropsied and processed for histology observation using immunohistochemistry staining.Results:CREM expression in rat Sertoli cells was not altered by the administration of either 0.2 or 0.4 ml seminal vesicle extract.Conclusion:The administration of seminal vesicle extract is unable to increase CREM expression in rat Sertoli cells.

show abstract

Human sperm anatomy and endocrinology in varicocele: role of androgen receptor

Cited by 19 publications

References 40 publications

A global view of the pathophysiology of varicocele

A global view of the pathophysiology of varicocele

The role of estradiol in male reproductive function

The expression of cyclic adenosine monophosphate responsive element modulator in rat sertoli cells following seminal extract administration

Contact Info

Product

Resources

About