Semen liquefaction failure is often caused by prostatitis.
Stubborn semen non-liquefaction is a pathological condition.
From the secretion of semen and ejaculation to the union of sperm and egg, it is a rather "twisted" process.
Normal semen is a milky white (pale yellow in those who have abstained from sex for too long) liquid with a distinctive odor, a mixture of secretions from the male accessory glands. 60% comes from the seminal vesicles, 30% from the prostate gland, and 10% from the epididymis, ampulla of the vas deferens, bulbourethral glands, and urethral glands. During ejaculation, semen is released from these glands in a specific sequence. Initially, a low-viscosity, milky white fluid containing a small number of sperm is released from the prostate gland; subsequently, a higher concentration of sperm is released along with secretions from the testes, epididymis, and vas deferens, as well as fluids from the prostate and seminal vesicles; finally, the seminal vesicle secretions complete the release. At the moment of ejaculation, under the influence of protein-like substances secreted by the seminal vesicles, this semen changes from a liquid state to a milky white or slightly yellow, translucent gel-like state. This change serves two purposes: preventing sperm from flowing out of the vagina and allowing the sperm to rest sufficiently. After 15-20 minutes, liquefaction factors (proteolytic enzymes secreted by the prostate gland) in the seminal plasma liquefy it into a thin, flowing liquid. Sperm, no longer hindered by the viscous state, have sufficient energy to penetrate cervical mucus and become more active, potentially reaching the fallopian tube to meet the egg and form a fertilized egg. Generally, semen that fails to liquefy after 30-60 minutes is considered to have non-liquefied semen. Good semen not only requires a good sperm count, sperm viability, and sperm motility, but also the quality of sperm forward movement and, more importantly, the finer sperm movements required to penetrate the cumulus oophorus and zona pellucida. Incomplete liquefaction of semen increases viscosity and prolongs liquefaction time, reducing sperm viability and motility. It also decreases sperm speed, linearity, and forward movement, increasing the number of sperm that remain stationary. This affects sperm penetration of cervical mucus, significantly hindering sperm movement within the female reproductive tract and preventing them from meeting the egg, thus preventing conception.
Inflammation of the prostate or seminal vesicles is the main cause of semen non-liquefaction; approximately 90% of patients with semen non-liquefaction have prostate dysfunction. Semen liquefaction mainly relies on proteolytic enzymes and other semen liquefaction factors produced by the prostate gland, which break down coagulation factors produced by the seminal vesicles. Prostatitis reduces the secretion of liquefaction factors, leading to insufficient fibrinolytic enzymes and deficiencies in trace elements (magnesium, zinc, etc.), gradually resulting in male semen non-liquefaction and affecting fertility. Specific causes also include infection and changes in seminal plasma composition.
Mycoplasma infection: Mycoplasma requires cholesterol and urea for growth, and the prostate gland is rich in cholesterol. Due to the prostate's anatomical location, urine easily refluxes into the prostate, providing it with the necessary urea. Therefore, the prostate is a common and major susceptible organ for mycoplasma. Mycoplasma cytoplasm contains urease, which can decompose urea to produce NH₃ and H₂O, causing cell damage and leading to prostatitis. This results in a deficiency of liquefaction factors, preventing the normal secretion of proteolytic enzymes, fibrinolytic enzymes, and other seminal liquefaction factors. This disrupts the coagulation factors produced by the seminal vesicles, leading to semen non-liquefaction and affecting fertility. Mycoplasma infection can also affect immunosuppressive substances in seminal plasma, leading to the production of antisperm antibodies.
Prostate-specific antigen (PSA) is essentially a chymotrypsin synthesized by prostate epithelial cells. It possesses chymotrypsin-like, trypsin-like, and esterase-like activities and is the most abundant protease in seminal plasma. Its physiological function is to degrade the main proteins in seminal fluid gel, thus liquefying the semen. After ejaculation, it is rapidly broken down by substances similar to PSA that have chymotrypsin-like activity. Prostatitis leads to a deficiency of PSA, which in turn causes abnormal semen liquefaction.
Acid phosphatase (ACP) in semen primarily originates from the prostate gland and is an important indicator of prostate function. Its physiological function is to hydrolyze substances in semen, such as phosphorylated choline, glycerol phosphate, and nucleotides, through phosphorylation to promote liquefaction. In addition to pathological changes in the prostate, chronic prostatitis is mainly characterized by a significant decrease in acid phosphatase secretion. Due to microscopic tissue hyperplasia, inflammatory cell infiltration, and glandular tubule obstruction caused by chronic prostatitis, ACP secretion is affected and reduced, clinically manifesting as abnormal semen liquefaction.
Urokinase is a proteolytic enzyme found in human semen, also known as urokinase-type plasminogen activator. The concentration of plasminogen activator in seminal plasma is 60-100 times higher than in blood. Secreted by numerous cells, it can affect semen liquefaction. As a plasminogen activator, it indirectly participates in the degradation of fibrinogen, thinning unliquefied or viscous semen, thus facilitating sperm forward motility. Therefore, decreased urokinase activity and levels may be one of the reasons for poor semen liquefaction.
Zinc is a crucial anti-infective factor in the prostate gland. In vitro experiments have confirmed its antibacterial effects against both Gram-positive and Gram-negative bacteria. Zinc in semen is primarily secreted by the prostate gland and participates in the synthesis of over 100 enzymes in the body. Normal semen liquefaction depends on the prostate gland secreting a normal amount of zinc to synthesize sufficient protease liquefaction factors. Normal concentrations of zinc in semen also stimulate sperm respiration and prolong lipid oxidation of sperm cell membranes, maintaining cell membrane stability and permeability, thus ensuring good sperm motility. In cases of chronic prostatitis, the zinc content in the prostate gland is significantly reduced, leading to a decrease in the synthesis and secretion of various proteases and liquefaction factors, resulting in semen non-liquefaction, decreased sperm motility, and male infertility.