Sleep restriction during peripuberty unbalances sexual hormones and testicular cytokines in rats.

Spermatogenesis and steroidogenesis are not fully established during puberty. Especially during this period, children and adolescents may be chronically sleep deprived due to early school hours and constant exposure to artificial light and interactive activities. We have previously shown that sleep restriction (SR) during peripuberty impairs sperm motility and has consequences on epididymal development in rats. Thus, this study aimed to evaluate the effect of SR during peripuberty on sexual hormones and its impact on testicular tissue. Rats were subjected to 18 h of SR per day for 21 days or were maintained as controls (C) in the same room. The circulating luteinizing hormone levels were decreased in SR rats without changes in the follicle stimulating hormone levels. Plasma and intratesticular testosterone and corticosterone in the SR group were increased in relation to C group. These alterations impair testicular tissue, with decreased IL-1ß, IL-6, and TNFα levels in the testis and diminished seminiferous epithelium height and Sertoli cell number. SR also increased testicular lipid peroxidation with no alteration in antioxidant profiles. There were no significant changes in sperm parameters, seminiferous tubule diameter, histopathology, spermatogenesis kinetics, neutrophil and macrophage recruitment, and IL-10 concentration. Our results show that SR unbalances sexual hormones and testicular cytokines at a critical period of sexual maturation. These changes lead to lipid peroxidation in the testes and negatively influence the testicular tissue, as evidenced by diminished seminiferous epithelium height-with apoptosis of germinative cell-and Sertoli cell number.

A High Fat Diet during Adolescence in Male Rats Negatively Programs Reproductive and Metabolic Function Which Is Partially Ameliorated by Exercise.

An interaction between obesity, impaired glucose metabolism and sperm function in adults has been observed but it is not known whether exposure to a diet high in fat during the peri-pubertal period can have longstanding programmed effects on reproductive function and gonadal structure. This study examined metabolic and reproductive function in obese rats programmed by exposure to a high fat (HF) diet during adolescence. The effect of physical training (Ex) in ameliorating this phenotype was also assessed. Thirty-day-old male Wistar rats were fed a HF diet (35% lard w/w) for 30 days then subsequently fed a normal fat diet (NF) for a 40-day recovery period. Control animals were fed a NF diet throughout life. At 70 days of life, animals started a low frequency moderate exercise training that lasted 30 days. Control animals remained sedentary (Se). At 100 days of life, biometric, metabolic and reproductive parameters were evaluated. Animals exposed to HF diet showed greater body weight, glucose intolerance, increased fat tissue deposition, reduced VO2max and reduced energy expenditure. Consumption of the HF diet led to an increase in the number of abnormal seminiferous tubule and a reduction in seminiferous epithelium height and seminiferous tubular diameter, which was reversed by moderate exercise. Compared with the NF-Se group, a high fat diet decreased the number of seminiferous tubules in stages VII-VIII and the NF-Ex group showed an increase in stages XI-XIII. HF-Se and NF-Ex animals showed a decreased number of spermatozoa in the cauda epididymis compared with animals from the NF-Se group. Animals exposed to both treatments (HF and Ex) were similar to all the other groups, thus these alterations induced by HF or Ex alone were partially prevented. Physical training reduced fat pad deposition and restored altered reproductive parameters. HF diet consumption during the peri-pubertal period induces long-term changes on metabolism and the reproductive system, but moderate and low frequency physical training is able to recover adipose tissue deposition and reproductive system alterations induced by high fat diet. This study highlights the importance of a balanced diet and continued physical activity during adolescence, with regard to metabolic and reproductive health.

Low doses of bisphenol A can impair postnatal testicular development directly, without affecting hormonal or oxidative stress levels.

Bisphenol A (BPA) is considered a potent endocrine disruptor, causing changes in the endocrine system due to its oestrogenic activity. Male individuals may be susceptible to endocrine, morphological and physiological alterations during testicular postnatal development. The aim of the present study was to evaluate whether exposure to BPA during the peripubertal period can damage testicular development. To this end, male Wistar rats were treated with BPA via gavage at doses of 20 or 200µgkg-1 on Postnatal Days (PND) 36-66. The control group was treated with Oil+DMSO under the same conditions. On PND 67, rats were killed. The blood was collected for hormonal analysis, the testis for sperm count, oxidative stress, histopathological and immunohistochemical analyses for ki-67 and sperm of the vas deferens for morphological analysis. Both doses of BPA resulted in abnormal sperm morphology and seminiferous tubules, with the highest dose increasing the height of the germinal epithelium and reducing the number of spermatozoa at Stages IX-XIII of spermatogenesis. In conclusion, both doses of BPA administered during the peripubertal period impaired testicular development without any effects on hormone levels (luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone levels) or oxidative stress.

Sleep restriction in Wistar rats impairs epididymal postnatal development and sperm motility in association with oxidative stress.

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.

Spermatic and testicular damages in rats exposed to ethanol: influence of lipid peroxidation but not testosterone.

Chronic consumption of ethanol causes morphological and physiological changes in the reproductive system of mammals. Vitamin C has an antioxidant role in organisms by neutralizing the ROS (reactive oxygen species) produced by oxidizing agents and this vitamin has an important function in the male reproductive system. The aim of this study was to evaluate whether vitamin C could prevent or attenuate the alterations in the male reproductive system caused by ethanol consumption. To test this hypothesis, male rats were divided into three experimental groups and treated by gavage for 63 days. The ethanol (E) and ethanol+vitamin C (EC) groups received 2 g/kg of ethanol (25%v/v) daily. In addition to ethanol, the EC group received vitamin C at a dose of 100 mg/day, diluted in water. The control group (C) received only the vehicle. On the 64th experimental day, the animals were anesthetized and euthanized, and blood was collected for plasmatic hormonal analysis. The testis, epididymis, vas deferens, and seminal vesicles were removed and weighed. Sperm from the vas deferens was submitted to morphological and motility analysis. The testis and epididymis were used for oxidative stress and histopathological analysis, sperm count, morphometric analysis of the testis, and stereological analysis of the epididymis. The results showed that vitamin C has a protective effect in the testes of adult male rats, entirely normalizing the parameters of sperm count, spermatogenesis kinetics, lipid peroxidation levels, and sperm motility, as well as partially normalizing the histopathological damage in the testis, epididymis, and sperm morphology. Thus, we concluded that lipid peroxidation is a major mechanism by which ethanol affects the testes and sperm, whereas no plasmatic testosterone alterations were found.