Abnormal Semen Analysis Parameters: Na+, K+-ATPase and Ca2+ -ATPase Activity

Infertility in the male is the inability of an individual to make his partner pregnant which is due to the existence of abnormal semen analysis parameters in the male partner of a couple who are incapable of conceiving after one year of having regular insecure intercourse. It is a complicated process. For a male to make a female partner pregnant there are things that must occur which include; the male must produce a healthy sperm which depends on how the reproductive organ grew and formed during puberty, At least one of the testicles must be functioning for pregnancy to be achieved and also the body need to be producing testosterone and other male hormones that maintain and trigger the production of sperm.

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The sperm must be carried into the semen, and they must be enough. In case the number of sperm in the semen is little, they reduce the chances of the sperm fertilizing the partners egg. In situations where there is a low sperm count- usually less than 39 billion sperm per an ejaculate. Lastly, the sperm must be functional and motile, in the case of abnormality of the sperm where the sperm motility is abnormal a conditional referred to as asthenozoospermia, it may fail to reach or even penetrate the partners egg, and the etiology involves an array of biochemical and functional defects. Motility also encompasses the sperm structure and function of the sperm membrane, and the membrane has a crucial function of regulating balance of ion transport system (Jimenez et al. 2012)

The hormone homeostasis is controlled and determined by Na+, K+-ATPase, and Ca2+-ATPase, which exist in the plasma membrane of most cells which include the sperm cell. Na+, K+-ATPase is an ion pump that exists the plasma membrane which makes the Na+ and K+ exchange that occurs between the intracellular and extracellular respectively in most cells which include the sperm cell. The electrochemical gradients for Na+ and K+ that are engendered by the Na+, K+-ATPase are paramount to the for the sperm cell physiology. Also, Ca2+-ATPase is a pump that responsible for calcium homeostasis which is also crucial in maintaining calcium homeostasis which enables the sperm cell to function normally (Takahashi & Yamaguchi 1999).

Sperm motility disorder may be caused by the failure of Na+, K+-ATPase, and Ca2+-ATPase homeostasis failure. The extracellular calcium is found to be an inhibitor to a collection of motile ram spermatozoas ejaculated. In cases of the dependence of motility on the activities of glycolysis, inhibition rate is minimal while in the dependence of respirations mitochondrion the stimulation is inhibited by the Quercetin.

We used articles obtained from PubMed as our primary source of information. The search for information in PubMed was in two stages, in the first step we used the keyword Na+, K+-ATPase and Ca2+-ATPase to search and we obtained seven journal articles that matched our keyword. In stage two, the Na+, K+-ATPase a4, and PMCA4 were used for the determination of the keywords. As a result, it was an achievement after obtaining knowledge from three journal articles. In summation, we collected almost ten journal articles. We did analysis as we reviewed the articles and recorded the information and data obtained in the form of tables and reports.

RESULTS AND DISCUSSION

Table 1. List of Na+,K+-ATPase role in sperm motility

Study by Na+,K+-ATPase role in sperm motility Reference

[Jimenez et al. 2011] that stated ion homeostasis is controlled by the activity of Na+,K+-ATPase defining the sperm motility. (Kocak-Toker et al. 2002). NKA activity has been found in human spermatozoa, and its inhibition produces a significant reduction in sperm motility (Kocak-Toker et al. 2002, Woo et al. 2002, Sanchez et al. 2006). Mouse and human sperm incubated with ouabain have shown that selective inhibition of a4 is sufficient to significantly decrease sperm motility (Kocak-Toker et al. 2002, Woo et al. 2002, Sanchez et al. 2006). [Sanchez et al. 2006] Na+,K+-ATPase a4 isoform has unique functional properties and plays a crucial role in sperm motility. [Jimenez et al. 2012; Woo et al. 2000] The inhibition of Na+,K+-ATPase a4 isoform by ouabain reduces the sperm total motility. Table 2. List of Na+,K+-ATPase mechanism in sperm motility

Study by Na+,K+-ATPase mechanism in sperm motility Reference

(Kaplan 2002). This enzyme catalyses the exchange of cytoplasmic Na+ for extracellular K+ in a 3:2 ratio (Kaplan 2002). (Hamamah & Gatti 1998). NHE exchanges H+ from the cell for extracellular Na+, and plays an important role in the regulation of intracellular pH (Hamamah & Gatti 1998). Wong et al. 1981, Giroux-Widemann et al. 1991) It is well known that acidic intracellular pH leads to a reduction in sperm motility (Wong et al. 1981, Giroux-Widemann et al. 1991) Table 3. List of Ca2+-ATPase role in sperm motility

Study by Ca2+-ATPase role in sperm motility Reference

[Vignini et al. 2009] Calcium ion homeostasis in normal cell function is responsibility for calcium pump, which is performed by Ca2+-ATPase. Salvador et al. 2009 The plasma membrane Ca2+ pump (PMCA) is an ATPase that extrudes Ca2+ from the cell Salvador et al. 2009 (Swerdloff RS, et al. 2015) Inhibition of the sodium-potassium pump causes an increase in intracellular Na+ concentrations, which in turn causes the Na+/Ca2+ exchanger to slow, ultimately leading higher intracellular Ca2+ concentration Williams & Ford, 2003 Human sperm incubated with quercetin (an inhibitor of PMCA) show a reduction in motility [ HYPERLINK "http://www.ncbi.nlm.nih.gov/pubmed/?term=Schuh%20K%5BAuthor%5D&cauthor=true&cauthor_uid=15078889" Schuh et al. 2004] PMCA4 is found in principal piece of flagellum and has a certain errand in sperm motility and hyperactivity. [Prasad et al. 2004] PMCA4 dysfunction caused infertility in men. Table 4. List of Ca2+-ATPase mechanism in sperm motility

Study by Ca2+-ATPase mechanism in sperm motility Reference

Poburko et al. 2011 PMCA activates as Ca2+/H+ counter transport with a 1:1 stoichiometric proportion producing a large amount of calcium protons extrusion into the mitochondrial matrix and resulting in pH decrease. [Poburko et al. 2011] Boczek et al. 2014 Calcium ion homeostasis is also link to cell metabolism by mitochondria. [Boczek et al. 2014] Chalmers. 2008; McKenzie. 2004] The physiological and pathological calcium signals are modulated by the activity of mitochondria, i.e. by buffering the intracellular calcium ions and by synchronizing the Ca2+-dependent activation or inhibition of numerous processes. [Chalmers. 2008; McKenzie. 2004] Frieden. 2003

Malli. 2003 By acting as a transient calcium ion buffers, the mitochondria will alter the promulgation of calcium ion transport, modify the activity of plasma membrane channels and transporters [Frieden. 2003] and enable the restocking of intracellular calcium ion stores. [Malli. 2003] Reference

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