Mitochondrial ferritin deficiency reduces male fertility in mice

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<sup>-/-</sup>) with FtMt<sup>+/+</sup> mice. We found that the number of newborns per litter and the fertility rate were strongly reduced for the FtMt<sup>-/-</sup> 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<sup>-/-</sup> 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<sup>-/-</sup> mice were significantly lighter and contained a lower number of spermatozoa compared with the controls. Also, the ATP content of FtMt<sup>-/-</sup> spermatozoa was found to be lower than that of FtMt<sup>+/+</sup> spermatozoa. These data show that FtMt contributes to sperm epididymis maturation and to male fertility.

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