Abstract
Nonobstructive azoospermia (NOA), which results from defective spermatogenesis, is the absence of spermatozoa in the semen. NOA is a complex and multigenetic disorder that is caused by genetic and environmental factors. For the process of spermiogenesis to be fully completed, the functions of telomeres and their length in reproduction are crucial. In recent years, many studies have been published on how leukocyte telomere length might play an important role in the pathophysiology of azoospermia. They show that shorter leucocyte telomere length (LTL) is strongly associated with NOA and defective spermatogenesis. Telomeres preserve human gametogenesis and fertility while preventing chromosomal ends from eroding. The length of the telomere significantly determines how it functions. The proteins are unable to attach to telomeric regions and cannot perform capping at chromosomal ends once telomere shortening rises above a crucial threshold. It is important to include LTL evaluations as a precursor test in the treatment planning that can be created for azoospermic patients.