Cadmium (Cd) is one of the most important heavy metal toxicants, used throughout the world at the industrial level. It affects humans through environmental and occupational exposure and animals through the environment. The most severe effects of oral exposure to Cd on the male reproductive system, particularly spermatogenesis, have not been discussed. In this study, we observed the damage to the testes and heritable DNA caused by oral exposure to Cd. Adult male Sprague–Dawley rats were divided into four groups: a control group and three groups treated with 5, 10, and 15 mg Cd/kg/day for 17 days by oral gavage. Our results revealed that Cd significantly decreases weight gain in 10 and 15 mg/kg groups, whereas the 5 mg/kg groups showed no difference in weight gain. The histopathology showed adverse structural effects on the rat testis by significantly reducing the thickness of the tunica albuginea, the diameter of the tubular lumen, and the interstitial space among seminiferous tubules and increasing the height of the epithelium and the diameter of the seminiferous tubules in Cd treated groups. Comet assay in epididymal sperms demonstrated a significant difference in the lengths of the head and comet in all the 3 Cd treated groups, indicating damage in heritable DNA, although variations in daily sperm production were not significant. Only a slight decrease in sperm count was reported in Cd-treated groups as compared to the control group, whereas the tail length, percentage of DNA in head, and tail showed no significant difference in control and all the experimental groups. Overall, our findings indicate that Cd toxicity must be controlled using natural sources, such as herbal medicine or bioremediation, with non-edible plants, because it could considerably affect heritable DNA and induce damage to the reproductive system.

In this study, we explored the gene expression patterns of the pituitary gland and hypothalamus of Angus cows at different growth and developmental stages by deep sequencing and we identified genes that affect bovine reproductive performance to provide new ideas for improving bovine fertility in production practice. We selected three 6-month-old (weaning period), three 18-month-old (first mating period), and three 30-month-old (early postpartum) Angus cattle. The physiological status of the cows in each group was the same, and their body conformations were similar. After quality control of the sequencing, the transcriptome analyses of 18 samples yielded 129.18 GB of clean data. We detected 13,280 and 13,318 expressed genes in the pituitary gland and hypothalamus, respectively, and screened 35 and 50 differentially expressed genes (DEGs) for each, respectively. The differentially expressed genes in both tissues were mainly engaged in metabolism, lipid synthesis, and immune-related pathways in the 18-month-old cows as compared with the 6-month-old cows. The 30-month-old cows presented more regulated reproductive behavior, and pituitary CAMK4 was the main factor regulating the reproductive behavior during this period via the pathways for calcium signaling, longevity, oxytocin, and aldosterone synthesis and secretion. A variant calling analysis also was performed. The SNP inversions and conversions in each sample were counted according to the different base substitution methods. In all samples, most base substitutions were represented by substitutions between bases A and G, and the probability of base conversion exceeded 70%, far exceeding the transversion. Heterozygous SNP sites exceeded 37.68%.

(1) Background: Endometrial regulation is a necessary condition for maintaining normal uterine physiology, which is driven by many growth factors. Growth factors produced in the endometrium are thought to be related to the proliferation of endometrial cells induced by estradiol-17β (E₂). In this study, we found that E₂ can induce the secretion of brain-derived neurotrophic factor (BDNF) in Ishikawa cells (the cells of an endometrial cell line). Furthermore, Ishikawa cells were used in exploring the regulatory role of BDNF in endometrial cells and to clarify the potential mechanism. (2) Methods: Ishikawa cells were treated with different concentrations of BDNF (100, 200, 300, 400, and 500 ng/mL). The mRNA expression levels of various proliferation-related genes were detected through quantitative reverse transcription polymerase chain reaction, and the expression of various proliferation-related genes was detected by knocking out BDNF or inhibiting the binding of BDNF to its receptor TrkB. The expression levels of various proliferation-related genes were detected by performing Western blotting on the TrkB-ERK1/2 signaling pathway. (3) Results: Exogenous BDNF promoted the growth of the Ishikawa cells, but the knocking down of BDNF or the inhibition of TrkB reduced their growth. Meanwhile, BDNF enhanced cell viability and increased the expression of proliferation-related genes, including cyclin D1 and cyclin E2. More importantly, the BDNF-induced proliferation of the Ishikawa cells involved the ERK1/2 signaling pathway. (4) Conclusions: The stimulating effect of exogenous E₂ on the expression of BDNF in the uterus and the action of BDNF promoted the proliferation of the Ishikawa cells through the TrkB-ERK1/2 signal pathway.