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[Changes in sperm mitochondria in patients with asthenozoospermia]
M Piasecka1, L Wenda-Rózewicka, A Kozanecka
1Katedry i Zakładu Histologii i Embriologii PAM.
Objective:
To evaluate functional and ultrastructural alterations of the spermatozoa midpieces in patients with asthenozoospermia and to find a correlation between the damage of the midpieces and loss of sperm motility.
Material And Methods:
Routine, morphological assessment of the midpieces stained according to the Papanicolaou method, cytochemical study of the mitochondrial activity using reaction for the diaphorase/ NADH according to the Piasecka method and electron-microscopic investigation of the midpiece structures were performed.
Results:
The cytochemical reaction for diaphorase/NADH revealed disorders of the mitochondrial activity and subtle and drastic malformations in the spermatozoa midpieces. The unusually thickened midpieces contained the supernumerary mitochondria. In patients with severe asthenozoospermia, the damage of the accessory fibres and axonemal complex located in the midpiece, were obtained also.
Conclusion:
This study indicates that mitochondrial defects are one of the causes that may account for loss of sperm motility in the population of patients.
Insights
Mitochondrial defects in sperm midpieces are linked to reduced sperm motility in asthenozoospermia patients. This study highlights mitochondrial dysfunction as a key factor in male infertility.
Area of Science:
- Reproductive Biology
- Spermatozoa Ultrastructure
- Mitochondrial Function
Background:
- Asthenozoospermia, characterized by poor sperm motility, significantly impacts male fertility.
- The midpiece of spermatozoa, crucial for motility, houses mitochondria responsible for energy production.
Purpose of the Study:
- To investigate functional and ultrastructural changes in sperm midpieces of asthenozoospermia patients.
- To correlate midpiece damage with diminished sperm motility.
Main Methods:
- Morphological assessment using Papanicolaou staining.
- Cytochemical analysis of mitochondrial activity (diaphorase/NADH reaction).
- Electron microscopy for ultrastructural examination of midpiece components.
Main Results:
- Disordered mitochondrial activity and midpiece malformations were observed.
- Severe asthenozoospermia cases showed damage to accessory fibers and the axonemal complex.
- Abnormalities included thickened midpieces with supernumerary mitochondria.
Conclusions:
- Mitochondrial defects are identified as a significant cause of reduced sperm motility.
- Ultrastructural and functional midpiece abnormalities contribute to asthenozoospermia.