scholarly journals Evaluation of response to restraint stress by salivary corticosterone levels in adult male mice

2016 ◽  
Vol 78 (5) ◽  
pp. 775-780 ◽  
Author(s):  
Masakatsu NOHARA ◽  
Atsushi TOHEI ◽  
Takumi SATO ◽  
Hiromi AMAO
Animals ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 736 ◽  
Author(s):  
Wael Ennab ◽  
Sheeraz Mustafa ◽  
Quanwei Wei ◽  
Zengpeng Lv ◽  
Ngekure M.X. Kavita ◽  
...  

The objectives were to investigate whether restraint stress (which is known as a mixture of psychologic and physical stress) exerts negative effects on the stomach and spleen, and whether the phenolic compound resveratrol (RES) exerts any protective roles. Fifty adult male mice were divided into five groups, with 10 mice per group as follows: control (C), restraint stress (RS), RS with vehicle (RS + V), RS with 2 mg/kg of resveratrol (RS + 2 mg RES), and RS with 20 mg/kg of resveratrol (RS + 20 mg RES). Mice were restrained in conical centrifuge tubes for 4 h daily to establish the RS model. RS + 2 mg RES, RS + 20 mg RES, and RS + V groups were given an oral dose of resveratrol or vehicle for 15 consecutive days, while the control group was not exposed to restraint stress. Herein, we showed that restraint stress decreased body weight and food and water consumption in stressed groups RS and RS + V compared to controls, while the groups treated with resveratrol showed improvements. Moreover, restraint stress caused acute damage to the morphology of gastric cells and reduced the quantitative distribution of parietal cells along with their decreased size and diameter, pointing to gastritis or ulcer. Furthermore, the antibody against the apoptosis-inducing factor (AIF) was highly attached in the RS groups. Splenic size, weight, and length were also greatly augmented in the stressed groups compared to the controls, while these phenomena were not observed in the RS + 2 mg RES group. Our findings proved significant ameliorating effects of resveratrol against restraint stress in adult male mice.


2019 ◽  
Vol 42 (3) ◽  
pp. 740-754
Author(s):  
Heba Saad Eldien ◽  
Nashwa Mostafa ◽  
Ola Abd ElTawab ◽  
Hussein Hassan ◽  
Tarek Abd Elhamid ◽  
...  

Zygote ◽  
2020 ◽  
Vol 28 (2) ◽  
pp. 160-169 ◽  
Author(s):  
Jie Zhang ◽  
De-Ling Kong ◽  
Bin Xiao ◽  
Hong-Jie Yuan ◽  
Qiao-Qiao Kong ◽  
...  

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.


2012 ◽  
Vol 35 (4) ◽  
pp. 805-811
Author(s):  
Dorria A.M. Zaghloul ◽  
Esam Salah Kamel ◽  
Hekmat O. Abd el-Aziz ◽  
Mohammed A. Mahmoud

2021 ◽  
Vol 152 ◽  
pp. 105276
Author(s):  
Clémence Maupu ◽  
Julie Enderlin ◽  
Alexandre Igert ◽  
Myriam Oger ◽  
Stéphane Auvin ◽  
...  

Reproduction ◽  
2011 ◽  
Vol 141 (2) ◽  
pp. 207-216 ◽  
Author(s):  
Christelle Stouder ◽  
Ariane Paoloni-Giacobino

Endocrine-disrupting chemicals (EDCs), among which methoxychlor (MXC), have been reported to affect the male reproductive system. This study evaluates the possible deleterious effects of MXC on imprinted genes. After administration of the chemical in adult male mice or in pregnant mice we analyzed by pyrosequencing possible methylation defects in two paternally imprinted (H19 and Meg3 (Gtl2)) and three maternally imprinted (Mest (Peg1), Snrpn, and Peg3) genes in the sperm and in the tail, liver, and skeletal muscle DNAs of the adult male mice and of the male offspring. MXC treatment of adult mice decreased the percentages of methylated CpGs of Meg3 and increased those of Mest, Snrpn, and Peg3 in the sperm DNA. MXC treatment of pregnant mice decreased the mean sperm concentrations by 30% and altered the methylation pattern of all the imprinted genes tested in the F1 offspring. In the latter case, MXC effects were transgenerational but disappeared gradually from F1 to F3. MXC did not affect imprinting in the somatic cells, suggesting that it exerts its damaging effects via the process of reprogramming that is unique to gamete development. A systematic analysis at the CpG level showed a heterogeneity in the CpG sensitivity to MXC. This observation suggests that not only DNA methylation but also other epigenetic modifications can explain the transgenerational effects of MXC. The reported effects of EDCs on human male spermatogenesis might be mediated by complex imprinting alterations analogous to those described in this study.


2019 ◽  
Vol 479 ◽  
pp. 159-169 ◽  
Author(s):  
Jianyao Wu ◽  
Petra Henning ◽  
Klara Sjögren ◽  
Antti Koskela ◽  
Juha Tuukkanen ◽  
...  

2019 ◽  
Vol 66 ◽  
pp. 242-250 ◽  
Author(s):  
Hossein Amini-Khoei ◽  
Elaheh Haghani-Samani ◽  
Masoumeh Beigi ◽  
Amin Soltani ◽  
Gholam Reza Mobini ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document