Both selenium deficiency and excess impair male reproductive system via inducing oxidative stress-activated PI3K/AKT-mediated apoptosis and cell proliferation signaling in testis of mice

Selenium (Se) deficiency or excess impairs testicular development and spermatogenesis, while the underlying mechanisms in this regard remain unclear. This study was designed to explore the molecular biology of Se deficiency or excess in spermatogenesis in mice. Three-week-old male mice (n = 10 mice/...

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Published in:Free radical biology & medicine 2023-03, Vol.197, p.15-22
Main Authors: Xu, Zi-jian, Liu, Meng, Niu, Qin-Jian, Huang, Yu-Xuan, Zhao, Ling, Lei, Xin Gen, Sun, Lv-Hui
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Caspase 3 - metabolism
Cell Proliferation
Dietary selenium
Male
Mice
Oxidative Stress
Phosphatidylinositol 3-Kinases - genetics
Phosphatidylinositol 3-Kinases - metabolism
Proto-Oncogene Proteins c-akt - genetics
Proto-Oncogene Proteins c-akt - metabolism
Selenium - metabolism
Semen - metabolism
Signal Transduction
Sperm Motility
Sperm quality
Testis
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Summary:Selenium (Se) deficiency or excess impairs testicular development and spermatogenesis, while the underlying mechanisms in this regard remain unclear. This study was designed to explore the molecular biology of Se deficiency or excess in spermatogenesis in mice. Three-week-old male mice (n = 10 mice/diet) were fed with Se-deficient diet (SeD, 0.02 mg Se/kg), adequate-Se diet (SeA, 0.2 mg Se/kg), or excess-Se diet (SeE, 2.0 mg Se/kg) for 5 months. Compared with SeA, SeD reduced (P 
ISSN:0891-5849
1873-4596
DOI:10.1016/j.freeradbiomed.2023.01.024