Sperm motility

About: Sperm motility is a research topic. Over the lifetime, 13874 publications have been published within this topic receiving 416587 citations. The topic is also known as: sperm movement & GO:0097722.

Sperm motility: is viscosity fundamental to progress?

Abstract: The success of internal fertilization is reliant upon successful sperm migration through the female tract. Timely location of the oocyte in what is a complex three-dimensional, highly invaginated series of moist opposed surfaces is a challenge at which only tens of sperm ever succeed. In part this could be due to the differences in scale, with a 50 mm long cell facing a probable migration of well over 20 cm due to the complex architecture. Many groups have focused upon the role for a chemotactic 'attractive egg' effect in guiding sperm to increase numbers at the fertilization site. What most research has neglected to consider is the role that the viscosity of the mucous layers, which coat the entire tract and through which sperm must swim, plays in both sperm selection and ongoing modulation of their behaviour. From allow- ing sperm to enter through the cervix during the ovulation phase, to denying them entrance through action of the female contraceptive pill, viscous effects are fundamental in controlling the migrating sperm population throughout the tract. The physiological effects of viscosity are also crucial to consider when designing and extrapolating data from in vitro experiments to the in vivo situation.

Increased phosphorylation of AKAP by inhibition of phosphatidylinositol 3-kinase enhances human sperm motility through tail recruitment of protein kinase A.

Abstract: Sperm motility is regulated by a complex balance between kinases and phosphatases. Among them, phosphatidylinositol 3-kinase (PI 3-kinase) has been recently suggested to negatively regulate sperm motility (Luconi, M., Marra, F., Gandini, L., Lenzi, A., Filimberti, E., Forti, G. and Baldi, E. (2001). Hum. Reprod. 16, 1931-1937). We demonstrate the presence and activity of PI 3-kinase in human spermatozoa and have investigated the molecular mechanism(s) by which the PI 3-kinase inhibitor, LY294002, triggers an increase in sperm motility. PI 3-kinase inhibition results in an increase in intracellular cAMP levels and in tyrosine phosphorylation of the protein kinase A-anchoring protein AKAP3. These effects finally result in a stimulation of protein kinase A (PKA) binding to AKAP3 in sperm tails through the regulatory subunit RIIbeta. The increased binding of RIIbeta to AKAP3 induced by LY294002 is mainly due to tyrosine phosphorylation of AKAP3, since it is completely blocked by the tyrosine kinase inhibitor erbstatin, which also reverses the effects of LY294002 on motility and suppresses PKA-AKAP3 interaction. The requirement of PKA binding to AKAP3 for sperm motility is confirmed by the reduction of motility induced by an inhibitor of RIIbeta-AKAP3 binding, Ht31, whose effects on sperm motility and PKA binding to AKAP3 are reversed by LY294002. These results demonstrate that PI 3-kinase negatively regulates sperm motility by interfering with AKAP3-PKA binding, providing the first evidence of a molecular mechanism by which PKA can be targeted to sperm tails by interaction with tyrosine phosphorylated form of AKAP3.

Characterization of sperm motility in sea bass: the effect of heavy metals and physicochemical variables on sperm motility

Abstract: Computer assisted sperm analysis (CASA) was used to characterize the motility of sea bass Dicentrarchus labrax spermatozoa and to study the effect of several physicochemical variables and heavy metals on sperm swimming performance Duration of sperm motility in sea bass was very short (<50 s) During the first 20 s all the motility variables measured remained approximately constant, the velocity and linearity of the movement being maximum during this period, while both variables decreased sharply later While slight variations in pH did not significantly modify sperm swimming performance, changes in osmolality affected all the measured motility variables Two of the heavy metals tested, Cu

Role of reactive oxygen species in the pathogenesis of mitochondrial dna (mtdna) mutations in male infertility

Abstract: Infertility affects about 15 per cent married couples half of which may be attributed to men with low sperm motility (asthenozoospermia), low sperm count (oligozoospermia) or abnormal sperm morphology (teratozoospermia). As mitochondria are the energy source for initiation, differentiation and function of the germ cells, mutation in mitochondrial genome can impair the formation of mature spermatozoa. Mutations in mitochondrial genome are identified in patients with fertility problems. However, mitochondria are also both the source and target of reactive oxygen species (ROS). ROS are normally generated at low levels by human spermatozoa in order to perform its physiological function. However, if the generation of these reactive free radicals overwhelm the antioxidant defense system, this can lead to oxidative stress, which is characterized by mitochondrial and nuclear genome damage. So both ROS and mtDNA mutations are considered to be the major aetiological factors in a variety of human diseases including male infertility. Identification of novel mutations in mtDNA of infertile patients with supraphysiological levels of ROS are considered to be important to gain better understanding of the aetiology of idiopathic infertility. Early detection and prompt antioxidant therapy can prevent ROS induced DNA damage. This has far reaching impact if such men opt for assisted reproductive technology (ART)/in vitro fertilization.