The effect of vitamin D on sperm motility and the underlying mechanism

Vitamin D deficiency is a common health issue around the world. We therefore evaluated the associations of semen quality with both serum and seminal plasma vitamin D levels and studied the mechanisms underlying these by incubating spermatozoa with 1,25(OH)2D in vitro. Two hun dred and twenty-two men were in eluded in our study. Vitamin D was detected using an electrochemilumi nesce nee method. Spermatozoa used for in vitro experiments were isolated by density gradient centrifugation. Positive relationships of serum 25(OH)D with semen volume and seminal plasma fructose were identified. Seminal plasma 25(OH)D level showed no relationship with serum 25(OH)D level, while it was inversely associated with sperm concentration and positively correlated with semen volume and sperm kinetic values. In vitro, sperm kinetic parameters in creased after in cubation with 1,25(OH)2D, especially upon in cubation for 30 min with it at a concen tration of 0.1 nmol l-1. Under these in cubation conditions, the upward migratio n of spermatozoa in creased remarkably with increasing ade nosine triphosphate (ATP) con centratio n. The concentrati on of cyclic ade nosine mono phosphate (cAMP) and the activity of protei n kinase A (PKA) were both elevated, and the PKA inhibitor, N-[2-(p-Bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H89) reversed the in crease of ATP producti on. The conce ntrations of cytoplasmic calcium ions and n icotinamide adenine dinucleotide (NADH) were both enhanced, while mitochondrial calcium uniporter (MCU) inhibitor, Ruthenium 360 (Ru360) did not reverse the increase of ATP production. Therefore, seminal plasma vitamin D may be invoIved in regulating sperm motility, and 1,25(OH)2D may enhance sperm motility by promoting the synthesis of ATP both through the cAMP/PKA pathway and the in crease in in tracellular calcium ions.

Relation of size of seminal vesicles on ultrasound to premature ejaculation

Myriad biological factors have been proposed to explain premature ejaculation （PE）. However, data correlating PE with seminal vesicles （SVs） are sparse. The study aimed to evaluate the relationship between the size of SV and PE. The cross-sectional study included 44 outpatients with PE and 44 volunteers without PE, and the size of SV was compared. Self-estimated intravaginal ejaculatory latency time, the Premature Ejaculation Diagnostic Tool （PEDT）, the International Index of Erectile Function-15, and the National Institutes of Health-Chronic Prostatitis Symptom Index were used for assessment of symptoms. Compared to the control group, the PE group had significantly higher mean anterior-posterior diameter （APD） of SV （P 〈 0.001）. The optimal mean APD of SV cutoff level was 9.25 mm for PE. In the PE group, PEDT was also higher with a mean APD of SV ≥9.25 mm compared with mean APD of SV 〈9.25 mm. PEDT was significantly correlated with the mean APD of SV （r = 0.326, P = 0.031）. The seminal plasma proteins were compared between six PE and six matched control cases by mass spectrometry and it was shown that 102 proteins were at least 1.5-fold up- or down-regulated. Among them, GGT1, LAMC1, and APP were significantly higher in the PE group. These results indicated that men with a larger mean APD of SV might have a higher PEDT score. Transrectal ultrasound of SV should be considered in the evaluation of patients with premature ejaculation. SV might be a potential target for the treatment of patients with PE and ultrasound change in SV.