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Asthenozoospermia and the human sperm mid-piece
A J Mundy1, T A Ryder, D K Edmonds
1Department of Reproductive Medicine, Queen Charlotte's and Chelsea Hospital, London, UK.
Human Reproduction (Oxford, England)
|January 1, 1995
Summary
Men with asthenozoospermia, a cause of infertility, have significantly shorter sperm mid-pieces and fewer mitochondrial gyres. This mitochondrial deficit explains the poor sperm motility observed in these individuals.
Area of Science:
- Reproductive Biology
- Cell Biology
- Andrology
Background:
- Asthenozoospermia is a leading cause of male infertility, characterized by reduced sperm motility.
- The precise ultrastructural defects contributing to asthenozoospermia require further elucidation.
- Mitochondria are crucial for providing energy for sperm motility.
Observation:
- Quantitative comparison of sperm surface and ultrastructural features between asthenozoospermic men and fertile controls.
- Scanning electron microscopy revealed significantly shorter sperm mid-pieces in asthenozoospermic subjects.
- Transmission electron microscopy showed significantly fewer mitochondrial gyres in the mid-pieces of asthenozoospermic sperm.
Findings:
- Sperm mid-piece length was significantly reduced (P < 0.01) in asthenozoospermic individuals compared to fertile controls.
- Asthenozoospermic sperm exhibited a significant deficit in mitochondrial gyres (P < 0.001).
- Mid-piece width and tail length were comparable between the two groups.
Implications:
- The reduced number of mitochondrial gyres suggests impaired energy production, explaining poor sperm motility in asthenozoospermia.
- These findings highlight specific ultrastructural targets for understanding and potentially treating male infertility.
- Objective morphometric analysis provides a valuable tool for diagnosing and characterizing sperm dysfunction.