No abstract

Bisphenol A (BPA) is a synthetic non-steroidal oestrogen used in the production of plastics. BPA can cause alterations in the endocrine system of human beings and animals at varied stages of development. During puberty, altered morphological, sexual behaviour and completion of the epididymal development occur. Therefore, this study aimed to evaluate the effects of BPA on epididymal development during the peripubertal period of rats. Male Wistar rats were treated with BPA via gavage at doses of 20 μg/kg or 200 μg/kg per day [post-natal day (PND] 36-66). The control group received the vehicles under the same conditions. Feed and water were provided ad libitum. On PND 67, the epididymis was removed, weighed, divided into caput/corpus and cauda sections. It was then used for sperm count determination; histopathological and stereological evaluation; inflammatory cell enzymatic profiling (myeloperoxidase activity - MPO; N-acetylglucosaminidase - NAG); immunohistochemistry for IL-6; and evaluation of superoxide anion levels and malondialdehyde (MDA). Exposure to BPA at 200 μg/kg caused a significant increase of MPO activity and immunoreactivity to IL-6 (interleukin-6) as well as remodelling of tissue components in the caput/corpus and cauda regions of the epididymis. Under these experimental conditions, it is concluded that BPA alters post-natal epididymal development.

Alterations in the circadian cycle are known to cause physiological disorders in the hypothalamic–pituitary–adrenal and the hypothalamic–pituitary–gonadal axes in adult individuals. Therefore, the present study aimed to evaluate whether exposure of pregnant rats to constant light can alter the reproductive system development of male offspring. The dams were divided into two groups: a light–dark group (LD), in which pregnant rats were exposed to an LD photoperiod (12 h/12 h) and a light–light (LL) group, in which pregnant rats were exposed to a photoperiod of constant light during the gestation period. After birth, offspring from both groups remained in the normal LD photoperiod (12 h/12 h) until adulthood. One male of each litter was selected and, at adulthood (postnatal day (PND) 90), the trunk blood was collected to measure plasma testosterone levels, testes and epididymis for sperm count, oxidative stress and histopathological analyses, and the spermatozoa from the vas deferens to perform the morphological and motility analyses. Results showed that a photoperiod of constant light caused a decrease in testosterone levels, epididymal weight and sperm count in the epididymis, seminiferous tubule diameter, Sertoli cell number, and normal spermatozoa number. Histopathological damage was also observed in the testes, and stereological alterations, in the LL group. In conclusion, exposure to constant light during the gestational period impairs the reproductive system of male offspring in adulthood.

Good sleep quality has a direct effect on the activity of the neuroendocrine-reproductive control axis and oxidative stress. Thus, the aim of the present study was to evaluate whether sleep restriction (SR) during the peripubertal period impaired the postnatal development of the epididymis in Wistar rats. After 21 days SR (18h per day), epididymides were collected on Postnatal Day (PND) 62 for evaluation of oxidative stress markers, inflammatory profile, sperm count and histopathological and stereological analyses; in addition, the motility of spermatozoa from the vas deferens was examined. SR significantly increased lipid peroxidation and glutathione levels in the caput and cauda epididymidis, and increased levels of total radical-trapping antioxidant potential in the caput epididymidis only. Neutrophil migration to the caput or corpus epididymidis was decreased by SR, and the size of the luminal compartment in the 2A region and the epithelial compartment in the 5A/B region was also decreased. In these regions, there was an increase in the size of the interstitial compartment. The percentage of immotile spermatozoa was higher in the SR group. In conclusion, SR affects epididymal postnatal development, as well as sperm motility, in association with increased oxidative stress and a decrease in the size of the epithelial compartment in the cauda epididymidis.

Ethanol consumption is associated with spermatogenesis damage and testosterone level alterations. Alcohol remains the most commonly used substance among athletes and sports enthusiasts. This study evaluated whether resistance physical exercise can reduce the testicular damage caused by ethanol exposure. A total of 36 ethanol drinking (UChB) rats were divided into four groups: C (control rats), ETOH (ethanol consumption), ETOH + T (ethanol consumption + physical training), and T (group physical training). The physical training component of the T and ETOH + T groups was based on a resistance training model consisting of four sets of 10 jumps, with an increasing overload of 50-70% of the body weight attached to the chest three times per week. Rats in the ETOH and ETOH +T groups received 10% ethanol. At postnatal day 90, the rats were sacrificed. Blood sample was collected for hormonal analysis, and the testicles were weighed and processed for histopathological, morphometric, and immunohistochemical analyses. The ETOH group showed an increase in testosterone levels. The immunohistochemical of androgen receptor and the absolute weight of the testes were higher in the ETOH and ETOH + T groups, while the ETOH animals showed a decreased weight gain index. The number of abnormal seminiferous tubules increased in the ETOH and T groups compared to those in the control group (C); however, the association with treatment (ETOH + T group) prevented this effect and decreased caspase-3 production. In conclusion, these findings show that the combination of ethanol consumption and resistance physical exercise can prevent testicular damage in adult UChB rats.