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Mitochondrial ferritin deficiency reduces male fertility in mice
Federica Maccarinelli1, Maria Regoni1, Fernando Carmona1
1Molecular Biology Laboratory, Department of Molecular and Translational Medicine DMMT, University of Brescia, Viale Europa 11, 25123 Brescia, Italy.
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.
Insights
Mitochondrial ferritin (FtMt) plays a crucial role in male fertility. Deleting the FtMt gene in mice significantly reduced fertility rates and sperm count, highlighting its importance in sperm maturation.
Area of Science:
- Reproductive Biology
- Mitochondrial Biology
- Genetics
Background:
- Mitochondrial ferritin (FtMt) is a specialized form of ferritin localized within mitochondria.
- FtMt is notably abundant in testicular tissue, suggesting a potential role in male reproductive function.
Purpose of the Study:
- To investigate the specific function of mitochondrial ferritin (FtMt) in male fertility and sperm maturation.
- To determine the impact of FtMt gene deletion on reproductive parameters in mice.
Main Methods:
- Generation of FtMt gene-deletion mice (FtMt-/-) and comparison with wild-type controls (FtMt+/+).
- Controlled mating experiments to assess fertility rates and litter sizes.
- Analysis of testis and sperm morphology, sperm parameters, oxidative stress indices, cauda epididymis weight, sperm count, and spermatozoal ATP content.
Main Results:
- FtMt-/- males exhibited significantly reduced litter sizes and fertility rates compared to controls.
- No significant differences were observed in testis or sperm morphology, or in oxidative stress markers.
- FtMt-/- mice showed lighter cauda epididymides with fewer spermatozoa and lower ATP content in spermatozoa.
Conclusions:
- Mitochondrial ferritin (FtMt) is essential for male fertility, impacting sperm epididymis maturation.
- FtMt deficiency leads to reduced sperm count and lower spermatozoal ATP levels, affecting male reproductive success.
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