Mitochondrial ferritin deficiency reduces male fertility in mice
Federica Maccarinelli A , Maria Regoni A , Fernando Carmona A , Maura Poli A , Esther G. Meyron-Holtz A B and Paolo Arosio A CA Molecular Biology Laboratory, Department of Molecular and Translational Medicine DMMT, University of Brescia, Viale Europa 11, 25123 Brescia, Italy.
B Laboratory for Molecular Nutrition, Faculty of Biotechnology and Food Engineering, Technion-Israel Institute of Technology, Technion City, 32000 Haifa, Israel.
C Corresponding author. Email: paolo.arosio@unibs.it
Reproduction, Fertility and Development 29(10) 2005-2010 https://doi.org/10.1071/RD16348
Submitted: 20 July 2016 Accepted: 3 December 2016 Published: 9 January 2017
Abstract
Mitochondrial ferritin (FtMt) is a functional ferritin targeted to mitochondria that is highly expressed in the testis. To investigate the role of FtMt in the testis we set up a series of controlled matings between FtMt gene-deletion mice (FtMt–/–) with FtMt+/+ mice. We found that the number of newborns per litter and the fertility rate were strongly reduced for the FtMt–/– males, but not for the females, indicating that FtMt has an important role for male fertility. The morphology of the testis and of the spermatozoa of FtMt–/– mice was normal and we did not detect alterations in sperm parameters or in oxidative stress indices. In contrast, we observed that the cauda epididymides of FtMt–/– mice were significantly lighter and contained a lower number of spermatozoa compared with the controls. Also, the ATP content of FtMt–/– spermatozoa was found to be lower than that of FtMt+/+ spermatozoa. These data show that FtMt contributes to sperm epididymis maturation and to male fertility.
Additional keywords: ATP, spermatogenesis, sperm motility.
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