PURPOSE: To investigate the pathophysiological role of superoxide anion and total reactive oxygen species (ROS) production by the spermatozoa of men with varicocele and its relationship with varicocele grade and semen parameters. MATERIALS AND METHODS: This prospective study included 34 men with grade II–III varicocele, regardless of their fertility status. The control group consisted of 13 healthy men. Semen characteristics were examined according to the 2010 World Health Organization criteria. The swim-up method was used for sperm preparation. Total ROS and superoxide anion production was assayed by luminol- and lucigenin-dependent chemiluminescence (CL), respectively. RESULTS: The men with varicocele had significantly higher total ROS and superoxide anion levels than the healthy control subjects (2.9±0.4 relative light unit (RLU) vs. 2.4±0.1 RLU, p=0.001 for luminol-dependent CL and 2.8±0.4 RLU vs. 2.3±0.2 RLU, p=0.002 for lucigenin-dependent CL). Cases of grade III varicocele had significantly higher superoxide anion and total ROS levels than grade II cases and control subjects (p < 0.001). Superoxide anion and total ROS levels were negatively correlated with all semen parameters. CONCLUSIONS: The superoxide anion levels produced by spermatozoa were significantly higher in varicocele patients than in control subjects. ROS production was related to increased varicocele grade, impaired semen concentration, and abnormal morphology in men with varicocele. Our findings suggest that superoxide anion overproduction may be an important step in the cascade of ROS-related damage to spermatozoa, resulting in impaired semen parameters in patients with varicocele.
Fertility ; Humans ; Luminescence ; Male ; Methods ; Oxidative Stress ; Prospective Studies ; Reactive Oxygen Species ; Semen* ; Spermatozoa* ; Superoxides* ; Varicocele* ; World Health Organization

Background/Aims: Gastrointestinal motility changes contribute to development and maintenance of obesity. Nesfatin-1 (NES-1) is involved in central appetite control. The aim is to elucidate effects of NES-1 and high-fat diet (HFD) on gastrointestinal motility and to explore myenteric neuron expressions of tyrosine hydroxylase (TH), vasoactive intestinal peptide (VIP), and neuronal nitric oxide synthase (nNOS) in HFDinduced oxidative injury. Methods: Sprague-Dawley rats were fed with normal diet (ND) or HFD. Gastric emptying rate was measured following NES-1 (5 pmol/rat, intracerebroventricular) preceded by subcutaneous injections of glucagon-like peptide 1 (GLP-1), cholecystokinin 1 (CCK-1), and gastrin/CCK-2 receptor antagonists. In carbachol-contracted gastric and ileal strips, contractile changes were recorded by adding NES-1 (0.3 nmol/L), GLP-1, CCK-1, and gastrin/CCK-2 antagonists. Results: Neither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND- and HFD-rats, but only lucigenin-chemiluminescence was increased in HFD-rats. Vasoactive intestinal peptide (VIP) and TH immunoreactivities were depressed and nNOS immunoreactivity was increased in gastric tissues of HFD-rats, while VIP and TH were enhanced, but nNOS was reduced in their intestines. Conclusions HFD caused mild systemic inflammation, disrupted enteric innervation, enhanced gastric contractility, inhibited ileal contractility, and eliminated inhibitory effect of NES-1 on gastric motility.

Background/Aims: Gastrointestinal motility changes contribute to development and maintenance of obesity. Nesfatin-1 (NES-1) is involved in central appetite control. The aim is to elucidate effects of NES-1 and high-fat diet (HFD) on gastrointestinal motility and to explore myenteric neuron expressions of tyrosine hydroxylase (TH), vasoactive intestinal peptide (VIP), and neuronal nitric oxide synthase (nNOS) in HFDinduced oxidative injury. Methods: Sprague-Dawley rats were fed with normal diet (ND) or HFD. Gastric emptying rate was measured following NES-1 (5 pmol/rat, intracerebroventricular) preceded by subcutaneous injections of glucagon-like peptide 1 (GLP-1), cholecystokinin 1 (CCK-1), and gastrin/CCK-2 receptor antagonists. In carbachol-contracted gastric and ileal strips, contractile changes were recorded by adding NES-1 (0.3 nmol/L), GLP-1, CCK-1, and gastrin/CCK-2 antagonists. Results: Neither HFD nor NES-1 changed methylcellulose emptying, but NES-1 delayed saline emptying in cannulated ND-rats. Inhibitory effect of NES-1 on gastric emptying in ND-rats was reversed by all antagonists, and abolished in HFD-rats. In HFD-rats, carbachol-induced contractility was enhanced in gastric, but inhibited in ileal strips. HFD increased body weight, while serum triglycerides, alanine transaminase, aspartate aminotransferase, glucose, and levels of malondialdehyde, glutathione, myeloperoxidase activity, and luminolchemiluminescence in hepatic, ileal, and adipose tissues were similar in ND- and HFD-rats, but only lucigenin-chemiluminescence was increased in HFD-rats. Vasoactive intestinal peptide (VIP) and TH immunoreactivities were depressed and nNOS immunoreactivity was increased in gastric tissues of HFD-rats, while VIP and TH were enhanced, but nNOS was reduced in their intestines. Conclusions HFD caused mild systemic inflammation, disrupted enteric innervation, enhanced gastric contractility, inhibited ileal contractility, and eliminated inhibitory effect of NES-1 on gastric motility.