Why does dead sperm appear?

Necrozoospermia may be caused by reproductive system infections, varicocele, endocrine abnormalities, bad living habits, and exposure to environmental toxins. Necrozoospermia is mainly characterized by a significant decrease in the proportion of viable sperm in semen, and is usually diagnosed through semen analysis.

1. Reproductive system infection:

Inflammations such as prostatitis and epididymitis can change the composition of seminal plasma and directly damage the sperm cell membrane. Mycoplasma or chlamydia infection can induce the accumulation of reactive oxygen species, leading to sperm DNA fragmentation. Clinically, antibiotics are needed to treat the primary infection, and antioxidants such as vitamin E are used to improve sperm survival rate.

2. Varicocele:

Obstruction of scrotal venous return will lead to an increase in local temperature of the testicles and hypoxic damage to the testicular spermatogenic epithelium. Patients often experience swelling in the scrotum on the affected side, and in severe cases, vermiform veins can be seen. Under the microscope, abnormal symptoms such as vacuolation of the sperm head can be seen, which need to be treated by high spermatic vein ligation.

3. Endocrine abnormalities:

Insufficient secretion of pituitary gonadotropin or defective androgen receptors can interfere with the sperm maturation process. In patients with hypothyroidism, enzyme activity in the testicles is reduced, causing sperm mitochondrial energy metabolism disorders. Such patients are often accompanied by degeneration of secondary sexual characteristics such as loss of sexual desire and sparse beard.

4. Bad living habits:

Long-term smoking will cause the cadmium content in seminal plasma to exceed the standard and destroy the sperm acrosome enzyme activity. Alcoholism can lead to testicular atrophy, and daily alcohol intake of more than 40 grams can significantly increase the rate of abnormal sperm. Melatonin secretion disorder caused by staying up late will interfere with the proliferation cycle of seminiferous epithelial cells.

5. Environmental toxin exposure:

Organophosphorus pesticides irreversibly inhibit cholinesterase and inactivate sperm tail motor proteins. Environmental estrogens such as bisphenol A can mimic the effects of estradiol, leading to an increase in the apoptosis rate of spermatogenic cells. Polycyclic aromatic hydrocarbons in car exhaust can directly damage the double-stranded structure of sperm DNA.

It is recommended that men preparing for pregnancy undergo routine semen examinations 3-6 months in advance and avoid high-temperature exposure behaviors such as wearing tight pants and bathing in hot springs. You can increase your daily intake of zinc-rich foods such as oysters and pumpkin seeds, and maintain 150 minutes of moderate-intensity exercise every week. Those who come into contact with chemical raw materials must take strict precautions. Assisted reproductive technology intervention should be considered when the sperm DNA fragmentation rate exceeds 30%.