Mitochondria Quality Control and Male Fertility

Abstract

Mitochondria are pivotal to cellular homeostasis, performing vital functions such as bioenergetics, biosynthesis, and cell signalling. Proper maintenance of these processes is crucial to prevent disease development and ensure optimal cell function. Mitochondrial dynamics, including fission, fusion, biogenesis, mitophagy, and apoptosis, maintain mitochondrial quality control, which is essential for overall cell health. In male reproduction, mitochondria play a pivotal role in germ cell development and any defects in mitochondrial quality can have serious consequences on male fertility. Reactive oxygen species (ROS) also play a crucial role in sperm capacitation, but excessive ROS levels can trigger oxidative damage. Any imbalance between ROS and sperm quality control, caused by non-communicable diseases or environmental factors, can lead to an increase in oxidative stress, cell damage, and apoptosis, which in turn affect sperm concentration, quality, and motility. Therefore, assessing mitochondrial functionality and quality control is essential to gain valuable insights into male infertility. In sum, proper mitochondrial functionality is essential for overall health, and particularly important for male fertility. The assessment of mitochondrial functionality and quality control can provide crucial information for the study and management of male infertility and may lead to the development of new strategies for its management.

The Distribution of Boars Spermatozoa in Morphometrically Distinct Subpopulations after In Vitro Exposure to Radiofrequency Electromagnetic Radiation at 2500 MHz and Their Motility

“…FIRMAN and SIMMONS [ 46 ] reported that midpiece size is a predictor of swimming speed of Mus musculus domesticus spermatozoa. It is known that RF-EMR can cause cell/sperm apoptosis, and mitochondria are the main initiators of apoptosis [ 47 ]. In addition, RF-EMR promotes increased mitochondrial ROS production and expression of mitochondrial apoptotic markers [ 48 ] with decreased mitochondrial membrane potential [ 47 , 49 ].…”

“…It is known that RF-EMR can cause cell/sperm apoptosis, and mitochondria are the main initiators of apoptosis [ 47 ]. In addition, RF-EMR promotes increased mitochondrial ROS production and expression of mitochondrial apoptotic markers [ 48 ] with decreased mitochondrial membrane potential [ 47 , 49 ]. Although the exact mechanism of apoptotic changes in spermatozoa, and in somatic cells, is still unknown, one of the signs of apoptosis was described as typical cell shrinkage [ 50 ].…”

Sperm mitochondria dysfunction in response to testicular cancer

“…In sperm, the remaining mitochondria are concentrated in the midpiece, which is the most proximal region of the human sperm tail 20 . Mitochondria in human sperm are arranged in an end‐to‐end manner forming the structure known as the ‘mitochondrial sheath’ that wraps along the outer dense fibres of the sperm tail 21 . These mitochondria, which are similar in ultrastructure and function to those found in other cells, assume a shape known as the ‘mitochondrial capsule’ 22 .…”

“…Interestingly, the preferred pathway in sperm and the extent of its utilization vary among species, in the developmental stage of the germ cell during spermatogenesis and the physiological status of sperm 13 . During its final stage, referred to as spermiogenesis, particularly at the stage of elongated spermatids, OXPHOS is the main energy‐generating pathway 21 . This stage is characterized by extensive remodelling of the cell structure to form the sperm tail and the acrosome, both of which require a significant amount of ATP.…”

“…In addition, glycolysis comes into play to support specific sperm functions and processes that require rapid ‘bursts’ of energy. Glycolysis is particularly important during sperm capacitation, a process that occurs after sperm is released into the female reproductive tract 21,27 . However, it has been confirmed that spermatozoa exposed to a carbohydrate substrates‐free medium or inhibitors of glycolysis 27,28 showed no significant effect on motility.…”