Porcine reproductive and respiratory syndrome virus (PRRSV) causes a highly contagious disease that threatens the global swine industry. Recent studies have focused on the damage that PRRSV causes to the reproductive system of male pigs, although pathological research is lacking. Therefore, we examined the pathogenic mechanisms in male piglets infected with PRRSV. Gross and histopathological changes indicated that PRRSV affected the entire reproductive system, as confirmed via immunohistochemical analysis. PRRSV infected Sertoli cells and spermatogonia. To test the new hypothesis that PRRSV infection in piglets impairs blood - testis barrier (BTB) development, we investigated the pathology of PRRSV damage in the BTB. PRRSV infection significantly decreased the quantity and proliferative capacity of Sertoli cells constituting the BTB. Zonula occludens-1 and β-catenin were downregulated in cell - cell junctions. Transcriptome analysis revealed that several crucial genes and signalling pathways involved in the growth and development of Leydig cells, Sertoli cells, and tight junctions in the testes were downregulated. Apoptosis, necroptosis, inflammatory, and oxidative stress-related pathways were activated, whereas hormone secretion-related pathways were inhibited. Many Sertoli cells and spermatogonia underwent apoptosis during early differentiation. Infected piglets exhibited disrupted androgen secretion, leading to significantly reduced testosterone and anti-Müllerian hormone levels. A cytokine storm occurred, notably upregulating cytokines such as tumour necrosis factor-α and interleukin-6. Markers of oxidative-stress damage (i.e. H2O2, malondialdehyde, and glutathione) were upregulated, whereas antioxidant-enzyme activities (i.e. superoxide dismutase, total antioxidant capacity, and catalase) were downregulated. Our results demonstrated that PRRSV infected multiple organs in the male reproductive system, which impaired growth in the BTB.

BACKGROUND: We recently reported that extract prepared from the aerial part of Cichorium intybus L. (CE) possesses hepatoprotective, hypolipidemic, and hypoglycemic properties. This paper focuses on the effects of CE on the male rat reproductive system and the effects of this treatment on pregnancy and offspring development.
METHODS: The experimental male rats received 100 mg/kg bw/day, 500 mg/kg bw/day, and 1000 mg/kg bw/day of CE orally for 60 consecutive days. Rats that received tap water were used as controls. After treatment, we evaluated the effects of CE on the male reproductive system, fertility, and offspring development.
RESULTS: For CE-treated male rats, there was a significant increase in the (1) diameter of seminiferous tubules, (2) spermatogenic index, (3) number of total and motile spermatozoa, and (4) testosterone levels. Additionally, there was a decrease in the pre- and post-implantation death of the embryos in the CE-treated group. All pups born from CE-treated males demonstrated normal development.
CONCLUSIONS: CE treatment significantly improved male reproductive functions. No adverse effects on pregnancy and offspring development were observed when males were treated with CE. Further clinical evaluation of CE should lead to the development of a safe and effective phytodrug for treating male infertility.

In recent years, mounting evidence has highlighted a global decline in male semen quality, paralleling an increase in male infertility problems. Such developments in the male reproductive system are likely due to a range of environmental factors, which could negatively affect the outcomes of pregnancy, reproductive health, and the well-being of fetuses. Different environmental contaminants ultimately accumulate in riverbed sediments due to gravity, so these sediments are frequently considered hotspots for pollutants. Therefore, understanding the detrimental effects of river sediment pollution on human reproductive health is crucial. This study indicates male germ cells\' high vulnerability to environmental contaminants. There is a strong positive correlation between the concentration of complex accumulated pollutants from human activities and the reproductive toxicity observed in human testicular embryonic cell lines NCCIT and NTERA-2. This toxicity is characterized by increased levels of reactive oxygen species, disruption of critical cellular functions, genotoxic impacts, and the induction of cell apoptosis. This research marks a significant step in providing in vitro evidence of the damaging effects of environmental pollutants on the human male germline.

Male fertility has been declining in recent decades, and a growing body of research points to environmental and lifestyle factors as the cause. The widespread use of radiation technology may result in more people affected by male infertility, as it is well established that radiation can cause reproductive impairment in men. This article provides a review of radiation-induced damage to male reproduction, and the effects of damage mechanisms and pharmacotherapy. It is hoped that this review will contribute to the understanding of the effects of radiation on male reproduction, and provide information for research into drugs that can protect the reproductive health of males.

Orange Bombax ceiba (B. ceiba) is an indigenous plant, and its stamen is an important ingredient in traditional Lanna food. There are limitations in scientific reports on the effects of the biological activities of B. ceiba stamens on the male reproductive system. This study aims to investigate the phytochemical compounds of the orange B. ceiba stamen and its potential effect on the antioxidant properties and quality of cattle sperm treated with Fe. The orange BUE had the highest total phenolics, total tannins, total monomeric anthocyanins, and maximal antioxidant potential. The orange BAE had the highest concentration of total flavonoids. LC-QTOF/MS showed that the orange BUE contained the highest number of phytochemical compounds related to male reproductive enhancement. The orange BUE enhanced sperm motility, and both the orange BUE and the BAE enhanced sperm viability and normal sperm morphology via free radical scavenging. It might be suggested that B. ceiba stamens have benefits for sperm preservation, sperm quality, and increasing the economic value of local plants, and that they may be developed and used to guard against oxidative stress from cryodamage induced by frozen semen technology.

OBJECTIVE: The effect of sleep-related variables on the reproductive system has garnered attention in recent years. One of the mediators that reportedly plays an important role in the relationship between sleep disorders and the reproductive system is a disruption of the circadian rhythm. The aim of curent study is to investigate the effect of chronotype on morning semen quality.
METHODS: Three-hundred and fourteen patients who applied to the infertility clinic were included in the study. The patients filled a socio-demographic data form. The \"Pittsburg Sleep Quality Index (PSQI) was used to evaluate the sleep quality while the chronotypes of the patients were evaluated with the \"Morningness -Eveningness-Questionnaire (MEQ)\". Semen analyses and biochemical analysis for testosterone serum plasma level of all patients were performed.
RESULTS: Twenty-one patients were assigned as evening, 187 patients were assigned as intermediate, and 106 were assigned as morning chronotype. No statistically significant difference was identified in the comparison of the mean MEQ scores between patients with low and normal sperm concentrations(p = 0.884). A correlation analysis indicated the presence of a significant positive correlation between normal morphology and MEQ scores (r = 0.13, p < 0.05) and a negative corelation between the hours spent in bed and sperm concentration (r = -0.13, p < 0.05). A general linear model created with independent variables suggested that the presence of varicocele and MEQ scores had a significant effect on normal morphology.
CONCLUSIONS: The results of present study support that evening type could negatively affect sperm morphology; additionally, the time spent in bed also negatively affected sperm concentration.

Successful male fertilization requires the main processes such as normal spermatogenesis, sperm capacitation, hyperactivation, and acrosome reaction. The progress of these processes depends on some endogenous and exogenous factors. So, the optimal level of ions and essential and rare elements such as selenium, zinc, copper, iron, manganese, calcium, and so on in various types of cells of the reproductive system could affect conception and male fertility rates. The function of trace elements in the male reproductive system could be exerted through some cellular and molecular processes, such as the management of active oxygen species, involvement in the action of membrane channels, regulation of enzyme activity, regulation of gene expression and hormone levels, and modulation of signaling cascades. In this review, we aim to summarize the available evidence on the role of trace elements in improving male reproductive performance. Also, special attention is paid to the cellular aspects and the involved molecular signaling cascades.

The escalation of technological advancements, coupled with the increased use of hazardous chemicals, has emerged as a significant concern for human health. Exposure to environmental pollutants like heavy metals and pesticides (insecticides, herbicides and fungicides) is known to significantly contribute to various health problems, particularly affecting reproductive health. Disturbances in reproductive potential and reproductive toxicity in males are particularly worrisome. Existing literature suggests that exposure to these environmental pollutants significantly alters male reproductive parameters. Thus, it is imperative to thoroughly analyze, comprehend, and evaluate their impact on male reproductive toxicity. Oxidative stress and disruptions in redox equilibrium are major factors through which these pollutants induce changes in sperm parameters and affect the reproductive system. Insecticides, fungicides, and herbicides act as endocrine disruptors, interfering with the secretion and function of reproductive hormones such as testosterone and luteinizing hormone (LH), consequently impacting spermatogenesis. Additionally, heavy metals are reported to bio-accumulate in reproductive organs, acting as endocrine disruptors and triggering oxidative stress. The co-operative association of these pollutants can lead to severe damage. In this comprehensive review, we have conducted an in-depth analysis of the impact of these environmental pollutants on the male reproductive system, shedding light on the underlying mechanisms of action.

There are few scientific reports on the histology of the phallus of ratite birds. The aim of this study was to conduct a histochemical analysis to determine the distribution of smooth muscle cells and the volumetric density (Vv) of the fibres of the elastic system in the ostrich phallus. Adult ostriches, 14 months old, were used. The phalluses were fixed in Bouin\'s solution and then transferred to a buffered formalin solution. They were then processed using standard histological stains for paraffin and slices were obtained. The following techniques were performed: HE, Picrosirius red, Alcian Blue at pH 1.0 and 2.5. The Periodic acid-Schiff reagent and Weigert\'s Resorcin-Fuchsin with previous oxidation were performed. The M42 test system was used to quantify the elastic system fibres. For immunohistochemical analysis, an anti alpha smooth muscle actin monoclonal antibody was used. The surface of the phallus is covered by a non-keratinized stratified squamous epithelium, which becomes stratified cylindrical in the region of the spermatic sulcus. No glands associated with the connective tissue were observed. The Vv of the elastic system fibres was 4.75%. Smooth muscle cells were visualized only in the walls of blood vessels through immunostaining, with an absence in the lymphatic sinuses. Despite similarities with other birds, such as the presence of a fibrous external axis, a lymphatic core, and a spermatic groove, the ostrich phallus shows marked differences, including the absence of an elastic core, a non-keratinized lining epithelium, and the absence of glands throughout its extension.

There is a paucity of studies on the multigenerational reproductive toxicity of fine particle matter (PM2.5) exposure during pregnancy on male offspring and the underlying mechanisms. This study explored the effects of PM2.5 exposure during pregnancy on the spermatogenesis of three consecutive generations of male mouse offspring. We randomized pregnant C57BL/6 mice into the control group, the Quartz Fiber Membrane control group, and two experimental groups exposed to different concentrations of PM2.5 (4.8 and 43.2 mg/kg B.Wt.). Pregnant mice from experimental groups received intratracheal instillation of PM2.5 of different doses on a three-day basis until birth. F1 mature male offspring from PM2.5-exposed pregnant mice were mated with normal female C57BL/6 mice. Likewise, their F2 mature male followed the same to produce the F3 generation. The results showed that PM2.5 exposure during pregnancy led to decreased body and tail length, body weight, and survival rates, decreased sperm concentration and sperm motility, and increased sperm abnormality rates significantly in F1 male offspring. We barely observed significant impacts of PM2.5 on the birth number, survival rates, and index of testes in the F2 and F3 offspring. Further exploration showed that PM2.5 exposure during pregnancy caused the morphological abnormality of Sertoli cells, downregulated androgen receptor (AR) and connexin43, upregulated anti-Müllerian hormone (AMH), cytokeratin-18 (CK-18), caspase-3, and cleaved caspase-3, decreased thyroid-stimulating hormone (TSH) and testosterone (T), and increased triiodothyronine (T3) in F1 male mouse offspring. Overall, we hypothesize that PM2.5 exposure during pregnancy mainly negatively impacts spermatogenesis in the F1 offspring. The possible mechanism could be that PM2.5 exposure during pregnancy disrupts endocrine hormone release in the F1 generation, thereby influencing the maturation and proliferation of their Sertoli cells and hindering spermatogenesis. This study for the first time investigates the role of Sertoli cells in the reproductive toxicity of PM2.5 on offspring.