BackgroundObesity is rapidly becoming a worldwide epidemic that affects children and adults. Some studies have shown a relationship between obesity and infertility, but until now it remains controversial. Thus, the aim of the present study was to investigate the effect of high-fat diet-induced obesity on male reproductive parameters.MethodsIn a first experiment, male Wistar rats were fed a high-fat diet (HFD) or standard chow (SD) for 15, 30 or 45 weeks, after which they were evaluated by adiposity index, serum leptin levels, reproductive organ weights and sperm counts. In a second experiment, rats received HFD or SD only for 15 weeks, long enough to cause obesity. Sexual hormones and sexual behavior were evaluated in these animals, as well as fertility after natural mating. Another group of rats was submitted to motility analysis and fertility evaluation after in utero insemination.ResultsAfter 15, 30 or 45 weeks, HFD-fed animals presented significant increases in obesity index and serum leptin levels. Reproductive organ weights and sperm counts in the testis and epididymis were similar between the two groups at all timepoints studied. Sexual behavior was not altered by the diet regimen, and HFD fertility after natural mating was also similar to SD-fed animals. Intergroup testosterone levels were also comparable, but estradiol levels were increased in HFD rats. Furthermore, sperm quality was reduced in HFD animals as evidenced by their decreased percentage of sperm with progressive movement. This altered motility parameter was followed by a trend toward reduction in fertility potential after artificial in utero insemination.ConclusionsThe results reported herein showed that obesity can affect sperm quality, by reducing sperm motility, without affecting other sperm parameters. The low sperm quality caused a slight reduction in fertility potential, showing that obesity may lead to impairment in male fertility.

Cisplatin is one of the most widely used and effective chemotherapeutic agents for the treatment of several human malignancies. This study evaluated the effects of peri-pubertal cisplatin administration on several reproductive end-points and the reversibility of these effects in adulthood. Peri-pubertal Wistar male rats (45 days old) were divided into two groups: control (saline 0.9%) and cisplatin (1 mg ⁄ kg ⁄ day, 5 days ⁄ week, for 3 weeks, i.p.). The study was conducted in two steps and evaluations were performed at ages of 66 (post-pubertal age) and 140 (adult age) days on: (i) organ weights, serum gonadotropins and testosterone levels, sperm counts, motility and morphology, testicular histomorphometry, spermatogenesis kinetics, Sertoli cell number and in situ detection of apoptotic germ cells and (ii) sexual behaviour, fertility and intratesticular testosterone. At the end of cisplatin therapy, rats showed reductions in sperm production and reserves, sperm with progressive movement, tubular diameter, intratesticular testosterone and fertility potential, but increased numbers of TUNEL-positive seminiferous tubules, immotile sperm and pre-implantation losses compared with control. Moreover, cisplatin-treated post-pubertal rats displayed impaired testicular histopathology and sexual behaviour. Serum gonadotropins and testosterone levels, sperm morphology, spermatogenesis kinetics and Sertoli cell number were comparable between experimental groups at both ages. Alterations found in post-puberty were recovered at adulthood, except for sperm motility and damage to testicular histology. The persistence of these cisplatin effects, despite the unaltered fertility after natural mating in rats, may have implications for reproductive function of young boys undergoing cancer therapy, given the lower reproductive efficiency in human beings compared with rats.

No abstract

Monitoring exposure to xenobiotics by biomarker analyses, such as a micronucleus assay, is extremely important for the precocious detection and prevention of diseases, such as oral cancer. The aim of this study was to evaluate genotoxic effects in rural workers who were exposed to cigarette smoke and/or pesticides and to identify possible classification patterns in the exposure groups. The sample included 120 participants of both sexes aged between 18 and 39, who were divided into the following four groups: control group (CG), smoking group (SG), pesticide group (PG), and smoking + pesticide group (SPG). Their oral mucosa cells were stained with Giemsa for cytogenetic analysis. The total numbers of nuclear abnormalities (CG = 27.16 ± 14.32, SG = 118.23 ± 74.78, PG = 184.23 ± 52.31, and SPG = 191.53 ± 66.94) and micronuclei (CG = 1.46 ± 1.40, SG = 12.20 ± 10.79, PG = 21.60 ± 8.24, and SPG = 20.26 ± 12.76) were higher (p < 0.05) in the three exposed groups compared to the GC. In this study, we considered several different classification algorithms (the artificial neural network, K-nearest neighbors, support vector machine, and optimum path forest). All of the algorithms displayed good classification (accuracy > 80%) when using dataset2 (without the redundant exposure type SPG). It is clear that the data form a robust pattern and that classifiers could be successfully trained on small datasets from the exposure groups. In conclusion, exposing agricultural workers to pesticides and/or tobacco had genotoxic potential, but concomitant exposure to xenobiotics did not lead to additive or potentiating effects.