Mitochondrial ferritin deficiency reduces male fertility in mice
Identificadores
URI: http://hdl.handle.net/10481/47233DOI: 10.1071/RD16348
ISSN: 1031-3613
ISSN: 1448-5990
Metadatos
Afficher la notice complèteAuteur
Maccarinelli, Federica; Regoni, Maria; Carmona Rodríguez-Acosta, Fernando; Poli, Maura; Meyron-Holtz, Esther G.; Arosio, PaoloEditorial
CSIRO Publishing
Materia
ATP Spermatogenesis Ferritin Mitochondrial ferritin Sperm motility
Date
2017-01-09Referencia bibliográfica
Maccarinelli, F.; et al. Mitochondrial ferritin deficiency reduces male fertility in mice. Reproduction, Fertility and Development: online (2017). [http://hdl.handle.net/10481/47233]
Patrocinador
The work was partially supported by MIUR grant PRIN10–11 to P. A. and by Telethon grant GGP1099 to P. A.Résumé
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.