Effects of altered epididymal sperm transit time on sperm quality

Abstract

The epididymal sperm transit time seems to have an important role in the process of sperm maturation, and it seems that alterations to the transit can harm the process. The aim of the present work was to evaluate the influence of altered sperm transit time through the epididymis on sperm parameters and fertility of rats, as well as the role of testosterone in the alterations. Sprague-Dawley adult male rats were randomly assigned to four different groups and were treated for 12 days: (i) 10 microg/rat/day DES, to accelerate the transit; (ii) 6.25 mg/kg/day guanethidine sulphate, to delay the transit; (iii) same treatment as group 1, plus androgen supplementation; (iv) control animals received the vehicles. Guanethidine treatment delayed the sperm transit time through the epididymal cauda, provoking increased sperm reserves in this region. Animals exposed to DES showed an acceleration of sperm transit time in the epididymis, and consequently decreased sperm density in both epididymal regions, the caput-corpus and cauda, and diminished sperm motility. In both cases sperm production was not altered. Testosterone supplementation was able to restore the transit time to values close to normality, as they were higher than in the control rats. The same occurred in relation to sperm motility. Rats exposed to DES presented lower fertility after in utero artificial insemination using sperm collected from the proximal cauda epididymis. Therefore, it was concluded that the acceleration of rat sperm transit time appeared to harm normal sperm maturation, thus decreasing sperm quality and fertility capacity, in an androgen-dependent way.

Interpreting histopathology in the epididymis

“…48 It was concluded that androgen deprivation accelerated transit and compromised normal facets of sperm maturation in the epididymis. Fernandez et al 49 confirmed these results using diethylstilbestrol (DES) administered with or without exogenous androgen supplementation. Epididymal transit time was accelerated and the fertility of cauda epididymal sperm was compromised in the DES-exposed animals; exogenous androgen ablated these effects.From a histopathology perspective it is important to recognize that when epdidymal sperm transit is accelerated, sperm numbers in the cauda are significantly reduced compared to control.…”

“…We also speculate that the acceleration of sperm transit reduces the time available for the processes necessary for the maturation of sperm, which can compromise the function of the resulting sperm. 18,49,85 …”

Impairment on sperm quality and fertility of adult rats after antiandrogen exposure during prepuberty

“…sperm motility and fertilizing potential. Indeed, both chloroethylmethanesulphonate and hydroxyflutamide exposures were shown to result in significantly reduced fertility following in utero insemination [44,45]. It is therefore, reasonable to assume that the decrease in fertility observed in the present study is at least in part due to maturational compromise caused by accelerated sperm transit.…”

Epididymal contraction and sperm parameters are affected by clonidine

“…The putative relationship between the treatment with crescent doses with clonidine and hormonal or metabolic alterations is uncertain and needs further investigation. However, the reduction in epididymis weight may be related in part to the decrease in the in the sperm reserves induced by sperm transit time acceleration (Fernandez et al, 2008;Bellentani et al, 2011;Borges et al, 2013). Furthermore, it has been described that the a 2 -adrenoceptors mediate anti-lipolytic effects in fat cells, regulating the lipolysis induced by the activation of b-adrenoceptors (Lafontan & Berlan, 1995).…”

“…Changes on the sperm transit time through the epididymis impair the spermatozoa maturation process and induce oxidative stress, affecting the quantity and quality of spermatozoa (Gil-Guzman et al, 2001;Fernandez et al, 2008). The sperm transit time is modulated by androgens, spontaneous contractile activity of epididymal smooth muscle and autonomic (sympathetic and parasympathetic) nervous system (Sujarit & Pholpramool, 1985;Ricker, 1998;Chaturapanich et al, 1999).…”