Cuscuta chinensis flavonoids alleviate bisphenol A‐induced apoptosis of testicular cells in male mice offspring

Andrologia ◽  
2019 ◽  
Vol 51 (11) ◽  
Author(s):  
Yuanyuan Wei ◽  
Shuying Li ◽  
Chao Han ◽  
Yongzhan Bao ◽  
Wanyu Shi
Keyword(s):  
Bisphenol A ◽  
Male Mice ◽  
Testicular Cells ◽  
Cuscuta Chinensis ◽  
Induced Apoptosis

Restraint stress of male mice triggers apoptosis in spermatozoa and spermatogenic cells via activating the TNF-α system

Zygote ◽  
2020 ◽  
Vol 28 (2) ◽  
pp. 160-169 ◽  
Author(s):  
Jie Zhang ◽  
De-Ling Kong ◽  
Bin Xiao ◽  
Hong-Jie Yuan ◽  
Qiao-Qiao Kong ◽  
...  
Keyword(s):  
Psychological Stress ◽  
Restraint Stress ◽  
Semen Quality ◽  
Sperm Quality ◽  
Fertilization Rate ◽  
Seminiferous Tubules ◽  
Spermatogenic Cells ◽  
Male Mice ◽  
Testicular Cells ◽  
Tnf Α

SummaryStudies have indicated that psychological stress impairs human fertility and that various stressors can induce apoptosis of testicular cells. However, the mechanisms by which psychological stress on males reduces semen quality and stressors induce apoptosis in testicular cells are largely unclear. Using a psychological (restraint) stress mouse model, we tested whether male psychological stress triggers apoptosis of spermatozoa and spermatogenic cells through activating tumour necrosis factor (TNF)-α signalling. Wild-type or TNF-α−/− male mice were restrained for 48 h before examination for apoptosis and expression of TNF-α and TNF receptor 1 (TNFR1) in spermatozoa, epididymis, seminiferous tubules and spermatogenic cells. The results showed that male restraint significantly decreased fertilization rate and mitochondrial membrane potential, while increasing levels of malondialdehyde, active caspase-3, TNF-α and TNFR1 in spermatozoa. Male restraint also increased apoptosis and expression of TNF-α and TNFR1 in caudae epididymides, seminiferous tubules and spermatogenic cells. Sperm quality was also significantly impaired when spermatozoa were recovered 35 days after male restraint. The restraint-induced damage to spermatozoa, epididymis and seminiferous tubules was significantly ameliorated in TNF-α−/− mice. Furthermore, incubation with soluble TNF-α significantly reduced sperm motility and fertilizing potential. Taken together, the results demonstrated that male psychological stress induces apoptosis in spermatozoa and spermatogenic cells through activating the TNF-α system and that the stress-induced apoptosis in spermatogenic cells can be translated into impaired quality in future spermatozoa.

scholarly journals Fighting Bisphenol A-Induced Male Infertility: The Power of Antioxidants

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 289
Author(s):  
Joana Santiago ◽  
Joana V. Silva ◽  
Manuel A. S. Santos ◽  
Margarida Fardilha
Keyword(s):  
Male Infertility ◽  
Bisphenol A ◽  
Sperm Concentration ◽  
In Vivo Studies ◽  
Sperm Dna Damage ◽  
Testicular Cells ◽  
Low Concentrations ◽  
Sperm Dna ◽  
Male Reproductive Health

Bisphenol A (BPA), a well-known endocrine disruptor present in epoxy resins and polycarbonate plastics, negatively disturbs the male reproductive system affecting male fertility. In vivo studies showed that BPA exposure has deleterious effects on spermatogenesis by disturbing the hypothalamic–pituitary–gonadal axis and inducing oxidative stress in testis. This compound seems to disrupt hormone signalling even at low concentrations, modifying the levels of inhibin B, oestradiol, and testosterone. The adverse effects on seminal parameters are mainly supported by studies based on urinary BPA concentration, showing a negative association between BPA levels and sperm concentration, motility, and sperm DNA damage. Recent studies explored potential approaches to treat or prevent BPA-induced testicular toxicity and male infertility. Since the effect of BPA on testicular cells and spermatozoa is associated with an increased production of reactive oxygen species, most of the pharmacological approaches are based on the use of natural or synthetic antioxidants. In this review, we briefly describe the effects of BPA on male reproductive health and discuss the use of antioxidants to prevent or revert the BPA-induced toxicity and infertility in men.

Histone acetylation plays an important role in MC-LR-induced apoptosis and cycle disorder in SD rat testicular cells

Chemosphere ◽  
2020 ◽  
Vol 241 ◽  
pp. 125073 ◽  
Author(s):  
Yueqin Wang ◽  
Haohao Liu ◽  
Xiaohui Liu ◽  
Xiaofeng Zhang ◽  
Jinxia Wu ◽  
...  
Keyword(s):  
Histone Acetylation ◽  
Testicular Cells ◽  
Sd Rat ◽  
Induced Apoptosis

scholarly journals Aggressive behavior and serum testosterone concentration during the maturation process of male mice: the effects of fetal exposure to bisphenol A.

2003 ◽  
Vol 111 (2) ◽  
pp. 175-178 ◽  
Author(s):  
Keisuke Kawai ◽  
Takehiro Nozaki ◽  
Hiroaki Nishikata ◽  
Shuji Aou ◽  
Masato Takii ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Aggressive Behavior ◽  
Serum Testosterone ◽  
Maturation Process ◽  
Fetal Exposure ◽  
Male Mice ◽  
Testosterone Concentration

scholarly journals Reduced body weight at weaning followed by increased post-weaning growth rate interacts with part-per-trillion fetal serum concentrations of bisphenol A (BPA) to impair glucose tolerance in male mice

PLoS ONE ◽  
2018 ◽  
Vol 13 (12) ◽  
pp. e0208846 ◽  
Author(s):  
Julia A. Taylor ◽  
Jennifer M. Sommerfeld-Sager ◽  
Chun-Xia Meng ◽  
Susan C. Nagel ◽  
Toshi Shioda ◽  
...  
Keyword(s):  
Growth Rate ◽  
Body Weight ◽  
Glucose Tolerance ◽  
Bisphenol A ◽  
Serum Concentrations ◽  
Male Mice ◽  
Impair Glucose Tolerance ◽  
Reduced Body ◽  
Fetal Serum

scholarly journals Perinatal Bisphenol A Exposure in C57B6/129svj Male Mice: Potential Altered Cytokine/Chemokine Production in Adulthood

2010 ◽  
Vol 7 (7) ◽  
pp. 2845-2852 ◽  
Author(s):  
Steven D. Holladay ◽  
Shuo Xiao ◽  
Honglu Diao ◽  
Jamie Barber ◽  
Tomas Nagy ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Male Mice ◽  
Chemokine Production

Impaired lipid and glucose homeostasis in male mice offspring after combined exposure to low-dose bisphenol A and arsenic during the second half of gestation

Chemosphere ◽  
2018 ◽  
Vol 210 ◽  
pp. 998-1005 ◽  
Author(s):  
Dezhen Wang ◽  
Wentao Zhu ◽  
Sen Yan ◽  
Zhiyuan Meng ◽  
Jin Yan ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Glucose Homeostasis ◽  
Low Dose ◽  
Combined Exposure ◽  
Male Mice

Bisphenol A-induced apoptosis, oxidative stress and DNA damage in cultured rhesus monkey embryo renal epithelial Marc-145 cells

Chemosphere ◽  
2019 ◽  
Vol 234 ◽  
pp. 682-689 ◽  
Author(s):  
Jianqin Yuan ◽  
Yanbiao Kong ◽  
Mohammad Mehdi Ommati ◽  
Zhongwei Tang ◽  
Hong Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Rhesus Monkey ◽  
Bisphenol A ◽  
Induced Apoptosis

scholarly journals Multigenerational and transgenerational impact of paternal bisphenol A exposure on male fertility in a mouse model

2020 ◽  
Vol 35 (8) ◽  
pp. 1740-1752 ◽  
Author(s):  
Md Saidur Rahman ◽  
Won-Ki Pang ◽  
Do-Yeal Ryu ◽  
Yoo-Jin Park ◽  
Myung-Geol Pang
Keyword(s):  
Dna Methylation ◽  
Bisphenol A ◽  
Large Scale ◽  
Corn Oil ◽  
Sperm Count ◽  
Future Generations ◽  
High Dose ◽  
Male Mice ◽  
Paternal Exposure ◽  
Methylation Patterns

Abstract STUDY QUESTION How does paternal exposure to bisphenol A (BPA) affect the fertility of male offspring in mice in future generations? SUMMARY ANSWER Paternal exposure to BPA adversely affects spermatogenesis, several important sperm functions and DNA methylation patterns in spermatozoa, which have both multigenerational (in F0 and F1) and partial transgenerational (mainly noticed in F2, but F3) impacts on the fertility of the offspring. WHAT IS KNOWN ALREADY BPA, a synthetic endocrine disruptor, is used extensively to manufacture polycarbonate plastics and epoxy resins. Growing evidence suggests that exposure to BPA during the developmental stages results in atypical reproductive phenotypes that could persist for generations to come. STUDY DESIGN, SIZE, DURATION CD-1 male mice (F0) were treated with BPA (5 or 50 mg/kg body weight per day (bw/day)) or ethinylestradiol (EE) (0.4 μg/kg bw/day) for 6 weeks. Control mice were treated with vehicle (corn oil) only. The treated male mice were bred with untreated female mice to produce first filial generation (F1 offspring). The F2 and F3 offspring were produced similarly, without further exposure to BPA. PARTICIPANTS/MATERIALS, SETTING, METHODS Histological changes in the testis along with functional, biochemical and epigenetic (DNA methylation) properties of spermatozoa were investigated. Subsequently, each parameter of the F0–F3 generations was compared between BPA-treated mice and control mice. MAIN RESULTS AND THE ROLE OF CHANCE Paternal BPA exposure disrupted spermatogenesis by decreasing the size and number of testicular seminiferous epithelial cells, which eventually led to a decline in the total sperm count of F0–F2 offspring (P < 0.05). We further showed that a high BPA dose decreased sperm motility in F0–F2 males by mediating the overproduction of reactive oxygen species (F0–F1) and decreasing intracellular ATP (F0–F2) in spermatozoa (P < 0.05). These changes in spermatozoa were associated with altered global DNA methylation patterns in the spermatozoa of F0–F3 males (P < 0.05). Furthermore, we noticed that BPA compromised sperm fertility in mice from the F0–F2 (in the both dose groups) and F3 generations (in the high-dose group only). The overall reproductive toxicity of BPA was equivalent to or higher (high dose) than that of the tested dose of EE. LARGE SCALE DATA N/A. LIMITATIONS, REASONS FOR CAUTION Further research is required to determine the variables (e.g. lowest BPA dose) that are capable of producing changes in sperm function and fertility in future generations. WIDER IMPLICATIONS OF THE FINDINGS These results may shed light on how occupational exposure to BPA can affect offspring fertility in humans. STUDY FUNDING/COMPETING INTEREST(S) This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (Grant No. NRF-2018R1A6A1A03025159). M.S.R. was supported by Korea Research Fellowship Program through the NRF funded by the Ministry of Science and ICT (Grant No. 2017H1D3A1A02013844). There are no competing interests.

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