AIMTo assess laminin levels in the seminal plasma of infertile and fertile men, and to analyze the correlation of laminin levels with sperm count, age, sperm motility and semen volume.

METHODSOne hundred and twenty-five recruited men were equally divided into five groups according to their sperm concentration and clinical examination: fertile normozoospermia, oligoasthenozoospermia, non-obstructive azoospermia (NOA), obstructive azoospermia (OA) and congenital bilateral absent vas deferens (CBAVD). The patients' medical history was investigated and patients underwent clinical examination, conventional semen analysis and estimation of seminal plasma laminin by radioimmunoassay.

RESULTSSeminal plasma laminin levels of successive groups were: 2.82 +/- 0.62, 2.49 +/- 0.44, 1.77 +/- 0.56, 1.72 +/- 0.76, 1.35 +/- 0.63 U/mL, respectively. The fertile normozoospermic group showed the highest concentration compared to all infertile groups with significant differences compared to azoospermic groups (P<0.05). Testicular contribution was estimated to be approximately one-third of the seminal laminin. Seminal plasma laminin demonstrated significant correlation with sperm concentration (r = 0.460, P < 0.001) and nonsignificant correlation with age (r = 0.021, P = 0.940), sperm motility percentage (r = 0.142, P = 0.615) and semen volume (r = 0.035, P = 0.087).

CONCLUSIONSeminal plasma laminin is derived mostly from prostatic and testicular portions and minimally from the seminal vesicle and vas deferens. Estimating seminal laminin alone is not conclusive in diagnosing different cases of male infertility.

Adult ; Azoospermia ; physiopathology ; Fertility ; physiology ; Humans ; Infertility, Male ; physiopathology ; Laminin ; metabolism ; Male ; Oligospermia ; physiopathology ; Semen ; physiology ; Sperm Count ; Sperm Motility

AIMTo assess heme oxygenase-1 (HO-1) activity in the cavernous tissue of sildenafil citrate-treated rats.

METHODSOne hundred and ninety-two Sprague-Dawley male rats, divided into four equal groups, were investigated. Group 1, the control group, received regular animal chow; group 2 received sildenafil citrate by intragastric tube; group 3 received sildenafil and HO inhibitor (zinc protoporphyrin, ZnPP); and group 4 received sildenafil and nitric oxide synthase (NOS) inhibitor L-nitroarginine methyl ester (L-NAME). Twelve rats from each group were killed after 0.5 h, 1 h, 2 h and 3 h of drug administration. Then HO-1 activity, cGMP levels and NOS enzymatic activity in the cavernous tissues were estimated.

RESULTSIn cavernous tissue, HO-1 activity, NOS enzymatic activity and cGMP concentration increased significantly in sildenafil-treated rats compared to other groups throughout the experiment. Rats receiving either HO or NOS inhibitors showed a significant decrease in these parameters. HO-1 cavernous tissue activity and NOS enzymatic activity demonstrated a positive significant correlation with cGMP levels (r = 0.646, r = 0.612 respectively; P < 0.001).

CONCLUSIONThe actions of PDE5 inhibitor sildenafil citrate in the cavernous tissue are partly mediated through the interdependent relationship between both HO-1 and NOS activities.

Administration, Oral ; Animals ; Cyclic GMP ; metabolism ; Drug Interactions ; Drug Therapy, Combination ; Enzyme Inhibitors ; pharmacology ; Heme Oxygenase-1 ; antagonists & inhibitors ; metabolism ; Male ; NG-Nitroarginine Methyl Ester ; pharmacology ; Nitric Oxide Synthase ; metabolism ; Penis ; drug effects ; enzymology ; Piperazines ; pharmacology ; Protoporphyrins ; pharmacology ; Purines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Sildenafil Citrate ; Sulfones ; pharmacology ; Vasodilator Agents ; pharmacology

AIMTo assess seminal plasma anti-Müllerian hormone (AMH) level relationships in fertile and infertile males.

METHODSEighty-four male cases were studied and divided into four groups: fertile normozoospermia (n = 16), oligoasthenoteratozoospermia (n = 15), obstructive azoospermia (OA) (n = 13) and non-obstructive azoospermia (NOA) (n = 40). Conventional semen analysis was done for all cases. Testicular biopsy was done with histopathology and fresh tissue examination for testicular sperm extraction (TESE) in NOA cases. NOA group was subdivided according to TESE results into unsuccessful TESE (n = 19) and successful TESE (n = 21). Seminal plasma AMH was estimated by enzyme linked immunosorbent assay (ELISA) and serum follicular stimulating hormone (FSH) was estimated in NOA cases only by radioimmunoassay (RIA).

RESULTSMean seminal AMH was significantly higher in fertile group than in oligoasthenoteratozoospermia with significance (41.5 +/- 10.9 pmol/L vs. 30.5 +/- 10.3 pmol/L, P < 0.05). Seminal AMH was not detected in any OA patients. Seminal AMH was correlated positively with testicular volume (r = 0.329, P = 0.005), sperm count (r = 0.483, P = 0.007), sperm motility percent (r = 0.419, P = 0.021) and negatively with sperm abnormal forms percent (r = -0.413, P = 0.023). Nonsignificant correlation was evident with age (r = -0.155, P = 0.414) and plasma FSH (r = -0.014, P = 0.943). In NOA cases, seminal AMH was detectable in 23/40 cases, 14 of them were successful TESE (57.5%) and was undetectable in 17/40 cases, 10 of them were unsuccessful TESE (58.2%).

CONCLUSIONSeminal plasma AMH is an absolute testicular marker being absent in all OA cases. However, seminal AMH has a poor predictability for successful testicular sperm retrieval in NOA cases.

Adult ; Anti-Mullerian Hormone ; Asthenozoospermia ; therapy ; Azoospermia ; therapy ; Follicle Stimulating Hormone ; analysis ; Glycoproteins ; analysis ; Humans ; Infertility, Male ; therapy ; Male ; Predictive Value of Tests ; Semen ; chemistry ; physiology ; Sperm Count ; Sperm Motility ; Spermatozoa ; physiology ; Testicular Hormones ; analysis ; Tissue and Organ Harvesting ; methods