DNA fragmentation in two cytometric sperm populations: relationship with clinical and ultrasound characteristics of the male genital tract

Abstract

We investigated whether DNA fragmentation in two cytometric sperm populations (PIdimmer and PIbrighter) with different biological characteristics and clinical relevance is related to clinical and color-Doppler ultrasound (CDUS) parameters of the male genital tract. One hundred and sixty males of infertile couples without genetic abnormalities were evaluated for clinical, scrotal, and transrectal CDUS characteristics, presence of prostatitis-like symptoms (with the National Institutes of Health-Chronic Prostatitis Symptom Index) and sperm DNA fragmentation (sDF) in PIdimmer and PIbrighter populations (using TUNEL/PI method coupled with flow cytometry). Data were adjusted for age (Model 1) along with waistline, testosterone levels, smoking habit, and sexual abstinence (Model 2). According to the statistical Model 2, PIdimmer sDF was associated with testicular abnormalities, including lower clinical and ultrasound volume (r = −0.21 and r = −0.20, respectively; P < 0.05), higher FSH levels (r = 0.34, P < 0.0001) and occurrence of testicular inhomogeneity (P < 0.05) and hypoechogenicity (P < 0.05). PIbrighter sDF was associated with prostate-related symptoms and abnormal signs, including higher NIH-CPSI total and subdomain scores, a higher prevalence of prostatitis-like symptoms and of CDUS alterations such as macro-calcifications, severe echo-texture inhomogeneity, hyperemia (all P < 0.05), and higher arterial peak systolic velocity (r = 0.25, P < 0.05). Our results suggest that DNA fragmentation in PIdimmer sperm, which is related to poor semen quality, mainly originates in the testicles, likely due to apoptosis. Conversely, DNA fragmentation in PIbrighter sperm appears to mainly originate during or after transit through the prostate, increasing with the presence of an inflammatory status of the organ. These results could lead to new perspectives for the identification of therapeutic targets to reduce sDF.

Does finasteride treatment for benign prostatic hyperplasia influence sperm DNA integrity in dogs?

“…Benign prostatic hyperplasia (BPH) is a reproductive disorder of men and dogs [1,2], with high prevalence in aged males [3,4]. The etiology of BPH is related to a hormonal imbalance between testosterone and estrogen and an increased activity of 5α-reductase, leading to higher dihydrotestosterone (DHT) concentrations [5].…”

“…Impaired spermatogenesis is often observed [7], which may affect sperm DNA integrity [8,9]. Sperm DNA damage related to BPH was previously described in dogs [3] and men [4], albeit not yet completely elucidated. It is suggested that biochemical modifications of the prostatic fluid play an important role on sperm damage.…”

Tracking research trends and hotspots in sperm DNA fragmentation testing for the evaluation of male infertility: a scientometric analysis

“…SDF can originate in both testicles and during sperm transit in the genital tract [7]. Increased levels of seminal apoptotic M540 bodies suggest disruption of spermatogenesis and testicular abnormalities [8].…”

Effects of FSH on Sperm DNA Fragmentation: Review of Clinical Studies and Possible Mechanisms of Action

“…Considering that viable, DNA fragmented spermatozoa are cells where DNA damage developed more recently respect to the ejaculation (28), these results suggest that oxidative stress acts later in sperm's life, most likely during transit in the male genital tract, whereas apoptotic damage occurs earlier, mainly at testicular level. A recent clinical study (36) seems to confirm such hypothesis revealing that sDF in unviable spermatozoa is associated mainly with the presence of ultrasound signs of testicular abnormalities, whereas the DNA fragmented sperm population containing viable spermatozoa was mostly associated with clinical and ultrasound alterations of the prostate and of seminal vesicles, likely due to inflammatory statuses. There is also evidence that DNA damage may occur after ejaculation during in vitro incubations (37–39) or because of in vitro manipulation during sperm selection for ARTs (33, 34, 40).…”