The article summarizes and analyzes published material related to the functioning and properties of passive ion-transporting systems in mammalian, in particular human spermatozoa. Transporting systems of Ca2+ and Na+ and their impact on sperm functional status and mammals fertility were described. Close attention was given to ion-transporting systems, the presence of which is proved in human spermatozoa.
Ion channels regulate the membrane potential and intracellular ionic concentration and thus serve a central role in various cellular processes. Several ion channels have been identified in the sperm plasma membrane, emphasizing their importance in male fertility and reproduction. They are essential for sperm motility, sperm activation, the acrosome reaction, and the journey toward the egg for fertilization.
The novel class of Ca2+ channels Catsper has been identified in human sperm and shown to be essential for mammalian hyperactivated sperm motility, sperm detachment from the female reproductive tract and egg coat penetration and fertility. Recent works suggest that CatSper may contribute to the [Ca2+]i increase that accompanies the acrosome reaction.
CatSper channels are constitutively active, weakly voltage-dependent, Ca-selective and strongly potentiated by intracellular alkalinization.
CatSper’s pore is formed by four α subunits Catsper1, Catsper2, Catsper3, Catsper4 and three auxiliary subunits – CatSperβ, CatSperγ, and CatSperδ. All four CatSper subunits (1–4) are needed for functional expression in mouse sperm, as knockout of any one of them results in absence of the other subunits in mature sperm with the consequent observation of male infertility and the lack of the CatSper associated currents. The absence of a single subunit may lead to degradation of remaining CatSper proteins.
Humans with mutations or deletions in CatSper1 and CatSper2 are infertile. It is suspected that loss-of-function mutations in any of the seven known CatSper subunits result in male infertility. CatSper1-/- male mice also display defects in cAMP and depolarization-induced calcium entry.
Other transporters appear as main candidates responsible for Ca2+ influx are voltagegated calcium channels CaVs. They convert changes of membrane potential into calcium signals. Though transcripts and proteins for both high voltage-activated and low voltage-activated types of CaV have been detected in mammalian sperm, electrophysiological evidence has mainly revealed the functional presence of CaV3 channels in mouse and human spermatogenic cells. It was proposed that they participate in acrosome reaction.
The presence of voltage-dependent Na+ channels NaV in human sperm was reported and supports a role for these channels in the regulation of mature sperm function. NaV channels could play a crucial role in noncapacitated sperm and in the initial capacitation steps.
ENaCs are present in mouse and human sperm. These channels may be regulated by рН, Са2+, Na+, Cl– and phosphorylation, parameters that change during capacitation. These channels are Na-selective, amiloride-sensitive and contribute to the resting membrane potential in cells by displacing it towards the Na+ equilibrium potential.
Mentioned ion channels control the sperm ability to fertilize the egg by regulating sperm maturation in the female reproductive tract and by triggering key sperm physiological responses required for successful fertilization such as hyperactivated motility, acrosome reaction.
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