scholarly journals Seminal fluid metabolome and epididymal changes after antibiotic treatment in mice

Reproduction ◽  
2018 ◽  
Vol 156 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Cheryl S Rosenfeld ◽  
Angela B Javurek ◽  
Sarah A Johnson ◽  
Zhentian Lei ◽  
Lloyd W Sumner ◽  
...  

Paternal environment can induce detrimental developmental origins of health and disease (DOHaD) effects in resulting offspring and even future descendants. Such paternal-induced DOHaD effects might originate from alterations in a possible seminal fluid microbiome (SFM) and composite metabolome. Seminal vesicles secrete a slightly basic product enriched with fructose and other carbohydrates, providing an ideal habitat for microorganisms. Past studies confirm the existence of a SFM that is influenced by genetic and nutritional status. Herein, we sought to determine whether treatment of male mice with a combination of antibiotics designed to target SFM induces metabolic alterations in seminal vesicle gland secretions (seminal fluid) and histopathological changes in testes and epididymides. Adult (10- to 12-week-old) National Institutes of Health (NIH) Swiss males (n = 10 per group) were treated with Clindamycin 0.06 mg/kg day, Unasyn (ampicillin/sulbactam) 40 mg/kg day and Baytril (enrofloxacin) 50 mg/kg day designed to target the primary bacteria within the SFM or saline vehicle alone. Fourteen-day antibiotic treatment of males induced metabolomic changes in seminal vesicles with inosine, xanthine and l-glutamic acid decreased but d-fructose increased in glandular secretions. While spermatogenesis was not affected in treated males, increased number of epididymal tubules showed cribriform growth in this group (7 antibiotic-treated males: 3 saline control males; P = 0.01). Antibiotic-treated males showed more severe cribriform cysts. Current findings suggest antibiotic treatment of male mice results in seminal fluid metabolome and epididymal histopathological alterations. It remains to be determined whether such changes compromise male reproductive function or lead to DOHaD effects in resulting offspring.

2020 ◽  
Vol 2020 ◽  
pp. 1-13 ◽  
Author(s):  
Xuejie Yi ◽  
Donghui Tang ◽  
Shicheng Cao ◽  
Tao Li ◽  
Haining Gao ◽  
...  

This study is aimed at investigating the effect of different exercise loads on the reproductive function of obese male mice and the underlying mechanisms. Male mice with high-fat diet-induced obesity were divided into obesity control (OC), obesity moderate-load exercise (OME), and obesity high-load exercise (OHE) groups. The OME and OHE groups were subjected to swimming exercise 5 days per week over a duration of 8 weeks, with the exercise load progressively increased to 2 h per day in the OME group and 2 h twice per day in the OHE group. In the OC group mice without exercise regimen, we observed a decrease in mRNA expression of antioxidant enzymes, increase in free radical products, upregulation of mRNA and protein expression of nuclear factor-κB and proinflammatory cytokines, inhibition of mRNA and protein expression of testosterone synthases, decrease in the serum testosterone level and sperm quality, and increase in sperm apoptosis. Although both moderate-load exercise and high-load exercise reduced body fat, only moderate-load exercise effectively alleviated obesity-induced oxidative stress, downregulated the expression of nuclear factor-κB and proinflammatory cytokines, and reversed the decrease in mRNA and protein expression of testosterone synthases, serum testosterone level, and sperm quality. These changes were not observed in the OHE group mice. Obesity-induced testicular oxidative stress and inflammatory response decreased testosterone synthesis and sperm quality. Moderate-load exercise alleviated the negative effect of obesity on male reproductive function by decreasing testicular oxidative stress and inflammatory responses. Although high-load exercise effectively reduced body fat, its effects on alleviating oxidative stress and improving male reproductive function were limited.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Angela B. Javurek ◽  
William G. Spollen ◽  
Amber M. Mann Ali ◽  
Sarah A. Johnson ◽  
Dennis B. Lubahn ◽  
...  

Abstract Bacteria harbored in the male reproductive system may influence reproductive function and health of the male and result in developmental origins of adult health and disease (DOHaD) effects in his offspring. Such effects could be due to the seminal fluid, which is slightly basic and enriched with carbohydrates; thereby, creating an ideal habitat for microbes or a potential seminal fluid microbiome (SFM). Using wild-type (WT) and estrogen receptor-alpha (ESR1) knockout (KO) male mice, we describe a unique SFM whose inhabitants differ from gut microbes. The bacterial composition of the SFM is influenced according to whether mice have functional Esr1 genes. Propionibacterium acnes, causative agent of chronic prostatitis possibly culminating in prostate cancer, is reduced in SFM of ESR1 KO compared to WT mice (P ≤ 0.0007). In certain genetic backgrounds, WT mice show a greater incidence of prostate cancer than ESR1 KO, which may be due to increased abundance of P. acnes. Additionally, select gut microbiome residents in ESR1 KO males, such as Lachnospiraceae and Christensenellaceae, might contribute to previously identified phenotypes, especially obesity, in these mutant mice. Understanding how genetics and environmental factors influence the SFM may provide the next frontier in male reproductive disorders and possibly paternal-based DOHaD diseases.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Martin Blomberg Jensen ◽  
Christine Hjorth Andreassen ◽  
Anne Jørgensen ◽  
John Erik Nielsen ◽  
Li Juel Mortensen ◽  
...  

AbstractInfertile men have few treatment options. Here, we demonstrate that the transmembrane receptor activator of NF-kB ligand (RANKL) signaling system is active in mouse and human testis. RANKL is highly expressed in Sertoli cells and signals through RANK, expressed in most germ cells, whereas the RANKL-inhibitor osteoprotegerin (OPG) is expressed in germ and peritubular cells. OPG treatment increases wild-type mouse sperm counts, and mice with global or Sertoli-specific genetic suppression of Rankl have increased male fertility and sperm counts. Moreover, RANKL levels in seminal fluid are high and distinguishes normal from infertile men with higher specificity than total sperm count. In infertile men, one dose of Denosumab decreases RANKL seminal fluid concentration and increases serum Inhibin-B and anti-Müllerian-hormone levels, but semen quality only in a subgroup. This translational study suggests that RANKL is a regulator of male reproductive function, however, predictive biomarkers for treatment-outcome requires further investigation in placebo-controlled studies.


1975 ◽  
Vol 78 (2) ◽  
pp. 373-384 ◽  
Author(s):  
J. Mauss ◽  
G. Börsch ◽  
K. Bormacher ◽  
E. Richter ◽  
G. Leyendecker ◽  
...  

ABSTRACT The effect of long-term testosterone administration on male reproductive function has been investigated in seven healthy young men age 20 to 27 years. Testosterone oenanthate (TOe) was administered in doses of 250 mg per week for 21 weeks. No toxic side-effects were observed. Libido, sexual potency, frequency of sexual intercourse and body hair development generally remained unaffected, but there was a reversible mean weight gain of 3.6 kg during TOe administration. Seminal fluid parameters and radioimmunoassayable serum FSH, LH, testosterone, and androstenedione levels were monitored before, during, and after TOe administration. The serum testosterone rose approximately by a factor of two, while the serum FSH and LH were rapidly suppressed after the initiation of the TOe therapy. The mean sperm concentration fell to values below three million spermatozoa per ml, and changes in sperm motility, the percentage of normal sperm morphology, and seminal fructose concentrations generally paralleled those of the mean sperm concentrations. In contrast, the mean seminal fluid volume and serum androstenedione levels did not change significantly during TOe administration. The mean sperm concentration showed a marked recovery 13 to 16 weeks after TOe withdrawal, but sperm counts remained below pre-treatment levels in three out of seven subjects 25 to 28 weeks after discontinuation of TOe.


2016 ◽  
Vol 8 (1) ◽  
pp. 101-112 ◽  
Author(s):  
S. O. Jeje ◽  
Y. Raji

Maternal treatment with dexamethasone (Dex) in threatening preterm delivery alters activities at the hypothalamic–pituitary–adrenal axis in the offspring. This alteration may interfere with reproductive function. The impact of gestational Dex exposure on male reproductive function of the offspring was investigated. A total of 25 pregnant rats randomly assigned to five groups (n=5) were treated with normal saline (control), Dex (100 μg/kg/day sc) during gestation days (GD) 1–7, 8–14, 15–21 and 1–21, respectively. Birth weight, anogenital distance (AGD), pubertal age, sperm parameters, hormonal profile and histopathology of testis and epididymis were determined in the F1 and F2 offspring. Results showed a significant increase (P<0.05) in pubertal age, serum corticosterone and gonadotropin-releasing hormone (GnRH) levels in the male offspring of DexGD 15–21 and 1–21 groups and a significant decrease (P<0.05) in serum testosterone, luteinizing hormone, birth weight and AGD at birth in the male F1 offspring. In the F2 offspring, there was a significant reduction (P<0.05) in serum corticosterone, testosterone, follicle-stimulating hormone and GnRH when compared with the control. Dex treatment at GD 15–21 and 1–21 significantly reduced (P<0.05) sperm motility and normal morphology in the F1 and F2 offspring. Maternal Dex treatment in rats during late gestation may disrupt sexual development markers in the F1 and F2 male offspring.


1990 ◽  
Vol 3 (3) ◽  
Author(s):  
S. Magnanelli ◽  
M. Wilks ◽  
T. Boake ◽  
S. Tabaqchali ◽  
J. A. H. Wass

2020 ◽  
Vol 16 ◽  
Author(s):  
Hamed Heydari ◽  
Rafighe Ghiasi ◽  
Saber Ghaderpour ◽  
Rana Keyhanmanesh

Introduction: Obesity resulted by imbalance between the intake of energy and energy consumption can lead to growth and metabolic disease development in people. Both in obese men and animal models, several studies indicate that obesity leads to male infertility. Objective: This review has discussed some mechanisms involved in obesity-induced male infertility. Method: Online documents were searched through Science Direct, Pubmed, Scopus, and Google Scholar websites dating from 1959 to recognize studies on obesity, kisspeptin, leptin, and infertility. Results: Obesity induced elevated inflammatory cytokines and oxidative stress can affect male reproductive functions including spermatogenesis disorders, reduced male fertility power and hormones involved in hypothalamus-pituitarygonadal axis. Conclusion: There is significant evidence that obesity resulted in male infertility. obesity has negative effect on male reproductive function via several mechanisms such as inflammation and oxidative stress.


2020 ◽  
Vol 20 (2) ◽  
pp. 198-202 ◽  
Author(s):  
Mohammad Motamedifar ◽  
Yalda Malekzadegan ◽  
Parisa Namdari ◽  
Behzad Dehghani ◽  
Bahia Namavar Jahromi ◽  
...  

Introduction: Infertility considered as a social and public health issue and estimated that most of these infertile couples are residents of developing countries. Infectious diseases including the history of Sexually Transmitted Infections (STIs) may impact on male reproductive function. Therefore, the present study aimed to investigate the prevalence of bacterial contaminants of semen and probable association with sperm quality of infertile men in Iranian population. Methods: The study population consisted of 200 infertile men and 150 fertile men attending an infertility Center in southwestern Iran during the study period in 2015. The assessment of sperm parameters was according to the World Health Organization (WHO) guidelines. The presumptive pathogens were identified using standard microbiology tests and confirmed by specific PCR primers. Results: The prevalence of bacteriospermia in the semen of the infertile group was significantly higher than that in the fertile group (48% vs. 26.7%, P <0.001). The microbiological analysis of samples showed that the most abundant species of bacteria in semen of infertile men were Chlamydia trachomatis (12.5%) followed by Neisseria gonorrhoeae (11%). On the other hand, in the control group, Lactobacillus spp. (17.3%) was the most isolated pathogen. Results showed that the presence of N. gonorrhoeae, C. trachomatis, Mycoplasma genitalium, Haemophilus, and Klebsiella was significantly associated with sperm abnormality. Conclusion: Based on our findings, it seems that bacteriospermia is associated with alterations in the properties of semen which may lead to a decrease in the fertilization potential of sperm. Therefore, immediate and appropriate treatment is necessary before investigating every other possible cause of infertility.


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