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Creatine phosphokinase in domestic cat epididymal spermatozoa*

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AbstractMammalian spermatozoa that have not completed final testicular sperm maturation have residual cytoplasm and increased creatine phosphokinase (CK) content. This study determined: (1) if CK could be detected by immunostaining cat spermatozoa from the caput, corpus, and cauda epididymis, (2) fluctuations in the proportions of spermatozoa with mature or immature CK‐staining patterns during epididymal sperm transit, and (3) how well sperm maturity (as determined by a CK marker) correlated with testicular or epididymal dysfunctions associated with morphological sperm abnormalities. One epididymis was collected from each of 37 cats after orchiectomy and processed immediately to allow sperm morphology evaluations on a ‘regional’ basis. Sperm released from the contralateral epididymis were evaluated for motility, sperm membrane integrity, and immunostaining with CK‐B antibodies. Proportions of spermatozoa with malformed or detached heads, proximal droplets and acrosomal or midpiece abnormalities decreased (P < 0.05) from the caput to the cauda epididymis. In contrast, proportions of spermatozoa that were motile, membrane‐intact or with flagellar abnormalities or distal droplets increased (P < 0.05) from the caput to cauda region. Percentages of spermatozoa with an immature CK‐staining pattern also decreased (P < 0.05) with epididymal transit (which differs from that reported for the human and stallion). There was no correlation (P > 0.05) between sperm morphology and the CK‐staining patterns. In summary, the results reveal that some specific sperm malformations in the domestic cat are of testicular origin, whereas others develop during epididymal transit. Mol. Reprod. Dev. 62: 265–270, 2002. © 2002 Wiley‐Liss, Inc.
Title: Creatine phosphokinase in domestic cat epididymal spermatozoa*
Description:
AbstractMammalian spermatozoa that have not completed final testicular sperm maturation have residual cytoplasm and increased creatine phosphokinase (CK) content.
This study determined: (1) if CK could be detected by immunostaining cat spermatozoa from the caput, corpus, and cauda epididymis, (2) fluctuations in the proportions of spermatozoa with mature or immature CK‐staining patterns during epididymal sperm transit, and (3) how well sperm maturity (as determined by a CK marker) correlated with testicular or epididymal dysfunctions associated with morphological sperm abnormalities.
One epididymis was collected from each of 37 cats after orchiectomy and processed immediately to allow sperm morphology evaluations on a ‘regional’ basis.
Sperm released from the contralateral epididymis were evaluated for motility, sperm membrane integrity, and immunostaining with CK‐B antibodies.
Proportions of spermatozoa with malformed or detached heads, proximal droplets and acrosomal or midpiece abnormalities decreased (P < 0.
05) from the caput to the cauda epididymis.
In contrast, proportions of spermatozoa that were motile, membrane‐intact or with flagellar abnormalities or distal droplets increased (P < 0.
05) from the caput to cauda region.
Percentages of spermatozoa with an immature CK‐staining pattern also decreased (P < 0.
05) with epididymal transit (which differs from that reported for the human and stallion).
There was no correlation (P > 0.
05) between sperm morphology and the CK‐staining patterns.
In summary, the results reveal that some specific sperm malformations in the domestic cat are of testicular origin, whereas others develop during epididymal transit.
Mol.
Reprod.
Dev.
62: 265–270, 2002.
© 2002 Wiley‐Liss, Inc.

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