Mitochondrial Membrane Potential Predicts 4-Hour Sperm Motility

Abstract

<jats:p>The evaluation of conventional and biofunctional sperm parameters is of fundamental importance for assessing male reproductive function. Among these, sperm motility is one of the most important parameters. Indeed, asthenozoospermia is a frequent cause of male infertility. Sperm motility depends on mitochondrial function and the measurement of mitochondrial membrane potential (MMP) better accounts for the function of this intracellular organelle. On the basis of these premises, the present study assessed whether the MMP predicts sperm motility at 4 h in patients with low or normal MMP. To accomplish this, 31 men were enrolled. Sperm analysis was conducted according to the WHO 2010 criteria. Particular attention was paid to the evaluation of MMP after liquefaction (T0) using JC-1 staining by flow cytometry. Sperm total and progressive motility were measured at T0 and after 4 h from seminal fluid collection (T4). Patients were divided into two groups based on their sperm mitochondrial function at T0. Group A (n = 18) was composed of men with normal mitochondrial function since they had a percentage of spermatozoa with low MMP (L-MMP) below the normal reference value of our laboratory (&lt;36.5%). In contrast, group B (n = 13) was made up of men with impaired sperm mitochondrial function (L-MMP &gt; 36.5%). Group A had a slight but not significant reduction in total and progressive sperm motility at T4 compared with the values recorded at T0. In contrast, patients in group B showed a significant decline in both total and progressive sperm motility at T4 compared with T0 (p &lt; 0.05). The results of this study showed that worse mitochondrial function, assessed by staining with JC1, is associated with a significant decline in sperm motility over time. These findings may be of clinical relevance in programs of assisted reproduction techniques. Based on our knowledge, there is no other evidence in the literature that has shown this relationship in healthy men with low MMP of idiopathic etiology, but normozoospermics according to the WHO 2010 criteria.</jats:p>

MRP5 and MRP9 play a concerted role in male reproduction and mitochondrial function

“…Loss of MRP5 and MRP9 alters mitochondrial homeostasis, not only inducing vacuolated and aberrant mitochondria but also resulting in a significant reduction in sperm mitochondrial membrane potential as observed by JC-1 staining. This relationship between mitochondrial membrane potential and sperm function directly correlates with mitochondrial health, sperm motility, and modulation of respiratory chain activity and oxidative phosphorylation pathways ( 27 , 81 , 86 – 88 ). Concordantly, male fecundity relies heavily on this organelle and its membranes being fully intact and functional for the overall health of the spermatozoa and their fertilization capacity, cementing why DKO males show such significant loss of biological function ( 27 , 80 – 82 ).…”

Staphylococcus-Induced Bacteriospermia In Vitro: Consequences on the Bovine Spermatozoa Quality, Extracellular Calcium and Magnesium Content

“…Similarly, a sperm agglutinating factor (SAF) was previously isolated from S. warneri and its recombinant version was recently proved as spermicidal in vitro, but also as an excellent contraception in vivo [ 27 ]. As mitochondrial membrane potential may predict 4-h sperm motility [ 28 ], intact mitochondria are an essential factor of sperm motion. Our research showed that semen samples infected mainly by S. aureus , S. warneri , S. cohnii , and S. kloosii were distinguished by the reduced mitochondrial membrane potential.…”

MRP5 and MRP9 Play a Concerted Role in Male Reproduction and Mitochondrial Function

“…Loss of MRP5 and MRP9 alters mitochondrial homeostasis not only inducing vacuolated and aberrant mitochondria, but also resulting in a significant reduction in sperm mitochondrial membrane potential as observed by JC-1 staining. This relationship between mitochondrial membrane potential and sperm function directly correlates with mitochondrial health, sperm motility, and modulation of respiratory chain activity and oxidative phosphorylation pathways (27, 82, 87–89). Concordantly, male fecundity relies heavily on this organelle and its membranes being fully intact and functional for the overall health of the spermatozoa and their fertilization capacity, cementing why DKO males show such significant loss of biological function (27, 81–83).…”