Responsiveness to progesterone and potassium channel blockers 4-aminopyridine, tetraethylammonium and free Ca(2+) contentration in spermatozoa of patients with oligozoospermia/leucocytospermia
The present study was undertaken to evaluate [Ca2+]i signals that occur in human sperm cells exposed in vitro to three diverse compounds; progesterone, 4-aminopyridine (a highly effective inducer of hyperactivation in human sperm) and tetraethylammonium. The [Ca2+]i reached after the extracellular c...
Gespeichert in:
Veröffentlicht in: | Ukrainian biochemical journal 2018-02, Vol.90 (1), p.48-57 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | The present study was undertaken to evaluate [Ca2+]i signals that occur in human sperm cells exposed in vitro to three diverse compounds; progesterone, 4-aminopyridine (a highly effective inducer of hyperactivation in human sperm) and tetraethylammonium. The [Ca2+]i reached after the extracellular calcium treatment was always higher in normozoospermic samples pretreated with progesterone than in pathozoospermic samples pretreated with progesterone. There were no changes in calcium signal in spermatozoa pretreated with progesterone from patients with oligozoospermia and leucocytospermia compared to control samples (without progesterone). [Ca2+]i. was always higher in pathozoospermic samples without 4-aminopyridine and always lower in pathozoospermic samples with 4-aminopyridine compared to these values in normozoospermic men. The 2 mM extracellular calcium administration to spermatozoa pretreated with tetraethylammonium did not result in a detectable increase in [Ca2+]i in normo- and pathozoospermic samples. The mechanisms of progesterone-dependent activation of the Ca2+-entry and the functioning of the voltage gated Ca2+-channels of plasmalemma are disturbed in pathologies – there was no increase in the Ca2+ level in the conditions of K+-depolarization (in the presence of inhibitors of K+-channels). |
---|---|
ISSN: | 2409-4943 2413-5003 |
DOI: | 10.15407/ubj90.01.048 |