Decreased motility of human spermatozoa presenting phosphatidylserine membrane translocation-cells selection with the swim-up technique

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Abstract

Phosphatidylserine membrane translocation (PST) is considered to be a marker of apoptosis; however, numerous studies have reported on its role in processes not related to cell death. The purpose of the study was to investigate: (1) what is the impact of PST on the motility of spermatozoa, and (2) does the swim-up isolation involve the percentage of cells presenting PST? Semen of 28 normozoospermic men (WHO criteria) was analyzed. High motility spermatozoa were isolated by the swim-up technique. The percentage of spermatozoa with PST in neat semen and after swim-up isolation was assessed with Annexin-V labeled with fluorescein, using flow cytometry technique. The spermatozoas' motility was measured with a computer-assisted analysis system. The kinetic subpopulations of spermatozoa were identified with dedicated software and analyzed regarding PST. Vital spermatozoa with PST demonstrated progressive movement. The motion analysis system revealed a very strong positive correlation between the percentage of vital spermatozoa with PST and the percentage of spermatozoa belonging to the slow subpopulation (r = 0. 83; p < 0. 05), as well as a very strong negative correlation between the percentage of vital spermatozoa with PST and the percentage of spermatozoa belonging to the rapid subpopulation (r = -0. 86; p < 0. 05). After the swim-up isolation, the percentage of vital spermatozoa presenting PST significantly decreased (2. 4 ± 2. 1% vs. 5. 2 ± 2. 4%; p < 0. 05). Spermatozoa with PST present progressive movement; however, their motility is decreased. Isolation of spermatozoa with the swim-up technique eliminates the cells with PST. © 2011 The Author(s).

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Kotwicka, M., Jendraszak, M., Skibinska, I., Jedrzejczak, P., & Pawelczyk, L. (2013). Decreased motility of human spermatozoa presenting phosphatidylserine membrane translocation-cells selection with the swim-up technique. Human Cell, 26(1), 28–34. https://doi.org/10.1007/s13577-011-0024-1

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