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Andrologia. 2018 Mar;50(2). doi: 10.1111/and.12848. Epub 2017 Jul 13.

Mitochondria-targeted antioxidant SkQ1 improves spermatogenesis in Immp2l mutant mice.

Jiang Y1,2, Liu C2,3,4, Lei B5, Xu X3,4, Lu B2.

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Department of Urology, Nanfang Hospital, Southern Medical University, Guangdong, China.
Wake Forest Institute for Regenerative Medicine, Wake Forest University Health Sciences, Winston-Salem, NC, USA.
Center for Reproductive Medicine, General Hospital, Ningxia Medical University, Ningxia, China.
Key Laboratory of Fertility Preservation and Maintenance, Ministry of Education, Ningxia Medical University, Ningxia, China.
Department of Urology, The First Affiliated Hospital of Jinan University, Guangzhou, China.


Previous studies have confirmed that spermatogenesis in homozygous Immp2l mutant male mice was normal at the age of 6 months, but was significantly abnormal at the age of 13 months. Meanwhile, oxidative stress is reported to be involved in spermatogenic impairment in old mutant mice. However, it is unclear whether antioxidant treatment is a suitable intervention for improving spermatogenesis in old mutant mice. This study sought to investigate the effect of mitochondria-targeted antioxidant SkQ1 on spermatogenesis in homozygous Immp2l mutant mice. Immp2l mutant mice were treated with the mitochondria-targeted antioxidant SkQ1 from the age of 6 weeks until 13 months. SkQ1 treatment significantly improved spermatogenesis in old Immp2 l mutant mice. Moreover, SkQ1 treatment improved the morphology of testicular seminiferous tubules, significantly reduced the apoptosis of germ cells and increased the level of GPX4 expression in old Immp2 l mutant mice. In conclusion, our data suggest that the mitochondria-targeted antioxidant SkQ1 is effective in improving spermatogenesis in Immp2 l mutant mice and might be used for the treatment of male infertility.


Immp2l mutant mice; SkQ1; male infertility; spermatogenesis

[Indexed for MEDLINE]

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